Numbers

 triglyceride<2
 Total cholesterol<5 (200)
 LDL<3.4 (100)
 HDL>1 (60)
 platelet value>150000-400000
 Mg 1.6-2.6
 k+ 3.5-5
 Na+ 135-145 (Na+ intake <3g/day)
 ca2+ 8.5-10
 Weight increased 3ibs/day, 5ibs/week indicates fluid retention,
HF.
 Digoxin 0.5-2 (hypokalemia/magnesemia, hypercalcemia cause
digoxin toxicity)
 BUN 5-20 (ACE/ARB restrict blood to kidneys, elevated BUN
means the medications damage the kidneys)
 Urine output (30ml/hr or 0.5-1.5ml/kg/hr)
 BNP>100 (B-type natriuretic peptide is measured to indicate heart
failure (when the ventricle is overstretched). >100= HF)
 Troponin I <0.6 normal, indicator for MI after 4hrs
 HB1AC <40 normal <40-50 pre
 Insulin 5-13
 glucose 3.5-5.4/100mg/dl (7.8/140mg/dl no fasting)
 lithium 0.5-1.2 (contraindicated with all dehydration, serious renal
dysfunctions, diuretics-hyponatremia <135 increase the risk of
lithium toxicity)
 BUN 5-20, creatine 0.6-1.2
 Partial thromboplastin time 25-35s, therapeutic 60-80s (can be
various but 1.5-2.5 times than normal)
 INR 2-3 (ideal therapeutic range for warfarin)
 Haematocrit (hameglobin/blood ration, 35-45%, signs for
bleeding/iron deficiency anemia)
 Haemoglobin counts 130-175/13-16
 Iron level 60-170 (10-30)
 MAP <60 (mean arterial pressure indicates the status of tissue
perfusion. usually 70-110, <60=hypovolemic shock, maintain >90
when neurogenic shock, >65 when septic shock)
 Ammonia (protein digestion byproduct-liver, 15-45, >45 cause
coma)
 Billirubin (RBC recycling byproduct, >1=juandice)
 Stroke volume (50-100ml per beat, depending on pre/afterload
and contractility)
 Cardiac output (4-8l/min)
 Blood composition (55 plasma+ 45% haemoglobin +1% platelets
and leukocytes)
 Haemoglobin (a protein carried by RBC to carry o2, 130-175)
 Uric acid >7/42
 Cardiac index 2.5-4l/min/m2 (<2.2 while having cardiogenic
shock)
 Pulmonary capillary wedge pressure=PCWP=PAWP= 4-12,
inserting a catheter to measure the L)atrial pressure. Used for
pulmonary odema/L) ventricular failure/mitral valve stenosis.
Pulmonary odema+ normal PCWP= acute respiratory distress
syndrome/non cardiogenic odema. low during hypovolemic shock
and high when cardiogenic shock (too much fluid retention)
 Central venous pressure 8-12
 Ejection fraction <40%= HF. Average EF 50-70%
 Paco2 38-42, >42 hypoventilation, <38-hyperventilation.
 Temperature 97-99
 Wbc 4-11
 Platelets 150-400
Heart blood flow

Superior/inferior vena cava- right atrium- tricuspid valve- right

ventricle- pulmonary semilunar valve- pulmonary artery –lungs-
pulmonary vein- left atrium- mitral (bicuspid) valve- left ventricle- aortic
semilunar valve- aorta.

The right coronary artery supplies the right atrium, ventricle and SA/AV
nodes. The left descending artery supplies the left ventricle, and the
circumflex artery supplies the left atrium.

HR

Increased HR= increased o2 demand= decreased cardiac output

The SA node is the primary pacemaker between the vena cava and the
right atrium. The sympathetic and parasympathetic system controls the
SA node, and the SA node generates impulses 60-100 times/min. AV
node is located in the atrial septum and receives impulses from the SA
node. If the SA node fails to generate impulses, the AV node can
generate impulses 40-60 times/min. The bundle of his connects
impulses to Purkinje fibres. Purkinje fibres are located in the ventricular
endocardium, propagating impulses to the ventricular myocardium to
contract. Purkinje fibres can generate their own impulse at 20-40
times/min.
Automatic nervous system

The sympathetic nerve fibres to release adrenaline

(bronchodilation/HR)/noradrenaline(vasoconstriction). The
nor/adrenaline neurotransmitter increases HR, SA node conduction,
ventricular contractility, and peripheral vasoconstriction. Thererfore
anticholinergic medications are used for overactive baldder or COPD (to
relax muscle)

The parasympathetic nerve fibres to release acetylcholine.

Acetylcholine is a neurotransmitter for positive cognitive functions by
working on hypothalamus, digest /rest and muscle contraction.
acetylcholine decreases HR, SA node conduction and ventricular
contractility.

Heart sound

 S1 when tricuspid and mitral valves close.

 S2 when pulmonary and aortic semilunar valves close.
 S3-- de,dedu (s1,23) indicates ventricular enlargement leading to
diastolic HF or regurgitation (thrombosis!!), could be normal for
pp younger than 18.
 S4 --dude,de (s41,2) happens when atrium systole and resistance
in the ventricle. S4 indicates cardio hypertrophy that ventricles
fails to eject all bloods (EF 50-75). Apical sound for s3/4.
BP management

Baroreceptors lower BP when hypertension more stimulation and

causing vasodilations , and stretch receptor increase BP when
hypotension causes more stimulation to produce ADH

Baroreceptors are located in the aortic arch and carotid sinus and
detect arterial BP changes. Increased arterial BP stimulates
baroreceptors to lower HR and vasodilation. Decreased arterial BP
causes less stimulation to baroreceptors, and HR goes up and
vasoconstriction.

Stretch receptors are located in the vena cava and right atrium. During
hypovolemic shock, stretch receptors stimulate the hypothalamus to
produce ADH (vasopressin) to increase water retention and
vasoconstriction.

Ventricular resistance is the determinant of distolic pressure. Atrial

resistance is the determinant of systolic pressure.

When measuring BP, the arm should be supported, bared, at heart

level, seat for more than 5mins, and 1hr after coffe/smoking.

Cardiomyopathy is a disease of cardiac muscle

Heart failure is when the heart cannot pump enough blood to meet
metabolic needs. So either the ventricle cannot contract enough
(systolic) or the ventricle is not properly refilled (diastolic). Usually, LHF
then RHF. EF<40%=HF=BNP>100. EF is tested by echocardiogram, heart
catheterization, and nuclear stress test. Forward failure refers to the
ejection cannot maintain organs perfusion. Backward failure refers to
fluid caused pressure building up in atrium etc. (pulmonary oedema).
Low output HF= forward failure. High output HF refers to the
myocardium that has to work strenuously to compensate. It

The causes of HF

Myocardial infarction is the most common cause of HF as myocardium

dies and no muscle to contract

Faulty valves like stenosis or regurgitation so the contraction would be

more rigorous (thrombosis risk)

Arrhythmia which could be caused by MI as the heart pumps too fast

(quivering) to be refilled

Lineage

Uncontrolled HTN
Recreational drugs

Evaders, rheumatic fever

LHF causes fluids building up in the lungs (pulmonary odema is the

most common symptom of LHF) and SOB. RHF causes fluids building up
in the peripheral parts like jugular or hepatic vein congestion and
oedema. Sitting patients in high fowler position (half/full set up) is the
best aid for breathing.

LHF mnemonic

1. Difficult to breath, hyperventilating cause low paco2 (hypocapnia)

<38-42
2. Rales
3. orthopnea
4. Weakness
5. Nocturnal paroxysmal dyspnea
6. Increased HR
7. Nagging cough- haemoptysis
8. Gained weight (2-3ibs/day, 5ibs/week)

RHF mnemonic
 1. Swelling
2. Weight gain
3. Edema
4. Lethargic
5. Large neck vein (jugular venous distention)
6. Irregular heartbeat (atrial fibrillation due to electrolytes
imbalance-hyperkalemia, catacholamine imbalance-too much
adrenaline beucase low return, myocardial necrosis? )
7. nocturia
8. Girth of abdomen increased
9. oliguria

Nursing intervention of HF

1. enhance myocardial oxygenation is the first priority. monitoring

breathing (no non selective bb/acei to cpod/asthma)/swelling
symptoms

2. orthostatic hypotension and high fall risk due to antiHTN meds

3.monitoring apical pulse before giving BB, jnitroglycerin, non-

bihydropyridine (amlodipine), digoxin

4. monitoring BP before giving ACEI, ARB, BB2, nitroglycerin, amiloride

(arteriole), isosorbide (venous), digoxin
5. Monitor UOP due to less tissue perfusion to the kidneys caused by
RHF. Also monitor BUN and creatine as ACEI and ARB limits blood
supply to the kidneys (BUN 5-20, creatine 0.6-1.2)

6. monitoring digoxin toxicity (loop/thiazide diuretics cause

hypokalemia and therefore digoxin toxicity 0.5-2)

7. monitoring lithium toxicity (all diuretics/NASIDs induced

hyponatremia 135-145/ dehydration/ kidney dysfunctions cause lithium
toxicity 0.5-1.2)

8. Monitor food/fluid intake at least two days after hospitalisation

9. Salt intake less than 3G and fluid restriction (<2L or whats the point
of taking diuretics)

10. Access sacral edema caused by RHF for bed ridden patients.

Angirogram is used to detect myocardial scarring and perfusion. Check

if the patient is allergic to iodine or shellfish before performing injection
dye for angiogram/angiography to prevent anaphylactic reactions.
Plapte pulses distal to the insertion site to evaluate potential vessel
occlusion.
Angina

Angina is chest tightness pain due to short oxygen supply. Preload,

afterload, contractility and HR increase oxygen demand and worsen the
angina. Sharp knife pain refers to the lungs during inspirations. Sit down
first when angina happens. Unstable angina is associated to MI mostly.

Variant (prinzmetal) angina refers to angina happens same time

everyday mostly morning even without precipitating factors.

Asking the patient if the pain is affecting by breathing.

The angina treatment goal is to reverse ischemia.

Coronary artery receives blood during diastole

Myocardial infraction

MI refers to no blood supply in myocardia tissues and die (necrosis).

Coronary artery thrombosis is the most common cause of MI. The most
common complication of MI is arrythmia. HF’s most common cause is
MI. A plaque in an artery (atherosclerosis is the name of the clot
building process) raptures causing a thrombus (a clot) and therefore
thrombosis. Thrombosis (arteries) or (arteries/veins) embolism refers
to a clot or other objects block the vessel) leads to a complete blockage
of a coronary artery (most common left anterior descending artery that
connects to left anterior/bottom of ventricle). After 20 mins (gold time)
of ischemia, the myocardial tissue starts to die (necrosis). This is the
most common cause of MI. Or coronary spasm (drugs) and coronary
dissection due to HTN (more likely in female). Neutrophiles are
presented in 24-36hrs after the MI. So, pericarditis is likely to happen as
neutrophiles (leukocytes) cause inflammation. The pericarditis can
further induce pericardial tamponade (jeopardise myocardial
contractility) and lead to another MI. Pericarditis can cause pericardial
effusion that fluids escape to the pericardial sac and causing same
effects. S&S of cardio tamponade are chest pain when lying flat or
coughing. Report fever, annorexia and night sweat as they are the signs
of pericarditis relapse. pericardiocentesis

S&S-CRUSHING

Chest pain

Radiating pain to jaw or arm

Unrelieved nitroglycerin chest pain

Sweating (hyperhidrosis)

Hard to breath (+RR)

Increased HR (+BP)

Nausea

Going to be anxious.

Nursing intervention

Once symptoms like chest pain show up, put 12 lead ECG on. ST-
segment elevation/depression, tall T waves/inversion indicate ischemia
or injury. monitoring BP/HR (in MI, the heart would find it harder to
pump, so the heart would bump faster and more strenuous, HR/BP), O2
supply on (2-4L) but only if the so2 is only lower than 95% (worsen the
symptom if o2 is given while the so2 is higher than 95%), preparing IV
accesses for meds, check respiratory sounds like rales (LHF leads to
pulmonary edema, crackles), strictly bedrest (prepare a urine bottle?),
collecting Troponin, administering meds while monitoring A/Es and
patient education. Check if the patient is allergic to iodine or shellfish
before performing angiogram/angiography to prevent anaphylactic
reactions. In the second day of hospitalisation, the pain is expected to
go away. Patients are only supposed to have small and easy digested
food. Low >2g sodium diet including tomato juice.

Meds for MI –acute angina means nasty artery blockage and cardiac
complications.

Antithrombosis

Heparin, an indirect thrombin inhibitor, (similar to clexane-lovenox,

enoxaparin, subcutaneous),IV, prevents blood clot formation rather
than platelets aggregation (antiplatelets) or dissolves clots (tissue
plasminogen activator or streptokinase, they contraindicated to
uncontrolled HTN, systolince >180). Heparin enhances the antithrombin
3 to slow thrombin activation (fibrinogen to fibrin conversion, fibrin
acts like a mesh to trap WBC/RBC etc). Monitor heparin-induced
thrombocytopenia (immune system forcibly active clotting process
incompletely, causes even more but tiny thrombus, diagnosed by
lowered the number of platelets (<150000) or half than platelets
baseline, s&s SOB, tenderness, swap to argatroban). Monitor bleeding
signs like black stools (positive stool guaiac test-GI bleeding), pink
urine-hematuria (renal bleeding), gum bleeding, decreased hemoglobin
and hematocrit and increasing HR/BP (the heart would pump more
strenuously to compensate for the heparin-induced blood loss),
monitoring partial thromboplastin time. Usually, partial thromboplastin
time is 30-40s, and the therapeutic range is 60-80s (the numbers could
be various but the therapeutic range is 1.5-2.5 times than normal).
Protamine is the antidote. Stop seven days before surgery due to the
risk of hemorrhage. Dabigatran (enteral only).

Antiplatelets

Aspirin (given for primaryly antithrombotic )and clopidogrel (plavix)

slows platelets agrégation but watch for GI bleeding (black stool). Stop
seven days before surgery. Clopidogrel rarely cause thrombotic
thrombocytopenia purpura and blocks blood supply to organs.

Morphine

The main purpose of administrating morphine is to decrease oxygen

demand of the heart by vasodilation if nitroglycerin doesn’t work or
calm patients down to lower o2 demand. But watch for low BP/HR/RR
as morphine is a depressant and potentially leading to respiratory
depression. It also relieves chest pain. Contraindicated to
benzodiazepines
Nitroglycerin

nitroglycerin vasodilates coronary arteries to deliver o2 but don’t give if

BP is lower than 90 and is contraindicated to phosphodiesterases like
sildenafil (viagra) or tadalafil (longer acting)can cause severe
hypotension. Giving sublingually in 5 mins intervals X3 maximum with
gloves on.

ACEI

ACEI vasodilates but causes nagging cough, might cause hyperkalemia

(3.5-5) and limits kidneys' blood supply (BUN 5-20, creatine 0.6-1.2).
ACEIs are ok for COPD

Beta blockers

Metoprolol or sotalol inhibits adrenaline. A/Es are low HR/BP and mask
the symptom of hypoglycemia (less glucose and high HR). Not for
COPD/asthma (bronchoconstriction), not with grapefruit juice

ARB

ARB is the same as ACEI, just no nagging cough (K+, kidney)

Cholesterol-lowering meds: statin

Statin lowers LDL (<3.4) and triglyceride (<2) and increases HDL (>1).
Monitor muscle pain and liver function(ALT/AST). Increased risk of
rhabdomyolysis when concurrent with fenofibrates (triglyceride
lowering). Excessive myoglobins in intravascular spaces can cause
kidney failure.

CCB

CCB cause negative inotropic, and chronotropic effects (diltiazem ,

verapamil) also vasodilations (filodipine) so monitor HR/BP,
constipation, HF (less contraction), and digoxin toxicity (0.5-2 CCB
increases the possibility), big gum but ok.

MI concurrent with digoxin kills.

ECG is the most common procedure to determine the location of

myocardial damage.
DVT

Venous thromboembolism is divided into deep vein thrombosis and

pulmonary embolism. DVT thrombus breaks off and flows to the lungs,
causing pulmonary embolism. DVT occasionally occurs in the upper
extremities but mainly in the calf and thigh (lower extremities),
including peroneal, posterior tibial, popliteal, and superficial femoral
veins.

DVT is caused by Virchow's Triad (SHE) and DVT causes venous

insufficiency.

1. Stasis of venous circulation.

When vein valves are damaged or muscle can't vasoconstriction, the

blood becomes static and coagulates. Immobilisation can waste the calf
muscle, varicose vein (a pool for stasis), hip/knee surgeries, LHF and
Atrial fibrillation.

2. Hypercoagulability

When septicemia, dehydration

3. Endothelial damage

Platelets get trapped in the damaged site—smoking and drugs in veins.

Patients with age (over 60), family history, obesity, smoking, atrial
fibrillation, myocardial infraction, contraceptive pills which includes
oestrogen and progestin/hormone therapy, and cancer (cause
hypercoagubility)/cancer treatment by using peripheral inserted central
catheter (PICC) or central venous catheter (CVC or port) are prone to
endothelial damage leading to DVT.

DVT signs

Redness, cyanosis, dull pain when mobolising, warmness, and swelling

are the DVT signs. Do compare with another extremity (using a tape
measure). Positive homans sign means dorsiflex of the foot towards the
knee and pain, but the positive homer sign could refer to various things.

Venography (dye injested to vein then xray) can see where the clots
are. D-dimer which access fibrin degradation fragments, tells if there
are blood clots. D-dimer can be given in different unit forms. >500
FEU=>250DDU= clots present. Duplex venous ultrasonography, MRI,
and Plethysmography

Prevention
Sequential compression devices (foot pumps) are cuffs on extremities
to push blood against the stasis. The cuffs must fit properly (asking the
pt if he feels the squeezing), changing regularly and wearing the cuffs
(as much as possible) unless the pt is mobilising. Never use SCD or
massage if the pt already has DVT. It could dislodge the clot and cause
an embolism in the left anterior descending artery, PE, stroke etc.
WORST SCENARIO!!

Compression stockings

Encourage pt out of bed and mobilising against stasis

No leg crossing or tight clothing.

When DVT presents:

 Elevated affected extremities above the heart level to promote

circulation (modified trendelenburg position-legs up body flat)
and reduce pain and oedema. If one extremity has DVT, then the
extremity would have longer capillary refill time and cyanosis.
 Ensure bed rest (ambulation can dislodge the clot just like
massage, SCD, and compression stockings. BIG NO!!!!!!)
 Applying warm compressions on the affected extremities.
 Access bilateral breath sounds in case pulmonary embolism
happens.
Heparin inhibits thrombin and, therefore, fibrinogen to fibrin
conversion (which acts like a mesh to trap things for clotting). Heparin
is fast onset, so sometimes heparin is concurrent with warfarin until
warfarin reaches INR 2-3 in around five days. Heparin dose depends on
the pt's weight and aPTT, and a therapeutic aPPT is 1.5-2.5 times more
than normal. If too low, clots are still forming. if the aPTT is too high,
hold the dose for an hour, then continue with the lowered dose.
Monitoring heparin-induced thrombocytopenia. In heparin-induced
thrombocytopenia, the immune system forcibly activates the clotting
process incompletely and causes many tinier thrombi also depletes
platelets. The symptoms are pain and swelling, and the platelet number
would be less than 150000 or less than half of the baseline platelet
number. You can swap to a direct thrombin inhibitor like argatroban.
The heparin antidote is protamine. Heparin can be given during
pregnancy. Long-term heparin cause osteoporosis (prone to fracture).
The injection site should be 5 inches away from the umbilicus and 2
inches from a scar. Don’t massage the injection area.

Warfarin antagonises vitamin K (clotting factor 10,9,7,2) as vitamin K is

used by the liver to create clotting factors. The antidote is vitamin K, so
watch for vitamin K food/supplement intake. Warfarin has a slow onset
of five days (until INR reaches 2-3). Can't be used during pregnancy as
the baby could birth defecet/hemorrhage. Warfarin is given enterally
and should be administered same time every day.

Heparin/warfarin needs to monitor aTTP 60-80 or 1.5-2.5 times than

baseline/INR2-3, platelet number, tachycardia and hypotension (due to
internal bleeding/relative hypovolemic shock, Hemoglobin
count/hematocrit-hemoglobin/blood ratio~40%), melena (positive stool
guaiac test refers to GI bleeding), haematuria, hematemesis (coffee
ground emesis), haemoptysis, gum oozing, and severe headache
(intercranial bleeding-haemorrhagic stroke). No garlic, green tea, and
gingko supplement.

IVC filter in vena cava stops clots from going to the heart. Only for
patients who are not candidates for anticoagulation or have recurrent
PE despite anticoagulation.
Shock refers to decreased tissue perfusion leading to cell hypoxia,
multiple organ dysfunction syndrome, and death.

In initial stage

Cells swap from aerobic metabolism to anaerobic metabolism due to

decreased cardiac output and o2 supply. Anaerobic metabolism makes
an excessive amount of lactic acid as a byproduct. The lactic acid
accumulation plus compromised liver function (decreased o2 supply)
cause tacidosis (ph 7.35-7.45. <7.35=acidosis). Subtle symptom.

Normal serum lactate <1, hyperlactatemia>2, acidosis >4

In the compensatory stage,

The baroreceptors in the carotid sinus and aortic arch (blood for the
brain and heart) detect lowered cardiac output (pressure). Then the
baroreceptors stimulate the sympathetic nervous system to release
adrenaline/noradrenaline. They will increase BP, HR, BSL,
bronchodilation and move fluid from the interstitial space to the
intravascular space. Also, more blood will be allocated to the heart and
brain than to other systems.

1. The reduction of blood to the kidneys will stimulate the beta 2

receptors of JG cells release renin-angiotensinogen-angiotensin 1-
angiotensin converting enzyme-angiotensin 2. Angiotensin 2 will
 vasoconstrict the vessels, stimulate the adrenal glands to release
aldosterone to keep sodium (therefore higher urine osmolarity-
urine concentration) and stimulate the pituitary gland to release
an antidiuretic hormone to vasoconstriction and making kidneys
keep water. Oliguria happens (<30ml/hr)
2. The GI will have less blood allocation leading to less peristalsis.
However, less peristalsis could increase the risk of rparalytic ileus,
so listen to bowel sounds, and the sound can't be absent.
3. The lungs would hyperventilate (high RR, <38paco2) to
compensate as some parts of the lungs lose their function (due to
less tissue perfusion).
4. The skin would have less perfusion and, therefore cold and
clammy (apart from distributive shocks
(neurogenic/anaphylactic/septicaemia, which causes vasodilation
systematically including integumentary areas).
5. The mental status are restlessness and apprehension.

In the progressive stage (major S&S show)

The efforts from the compensatory stage failed, and the cardiac output
is low again. Cells start to experience hypoxic injury, and the capillary
permeability is increased. Consequently, the fluid would flow back from
the intravascular space to the interstitial space and, therefore, oedema.
The mean arterial pressure (MAP) would be lower than 60 mmHg (MAP
is the index for tissue perfusion, usually 70-110, at least 60 to maintain
the minimal function of the human body)

1. In the brain, as the MAP <60, the cerebral perfusion pressure

decreases, and neurons die. This would deteriorate the patient’s
mental status (anxious, agitated and confused) and leading to no
reaction to environmental stimulation in refractory stage.
2. In the lungs, acute respiratory distress syndrome would happen.
an increased capillary permeability causes pulmonary oedema
(fluid retention) and Alveoli are collapsed as the interstitial fluid
squeezing the alveoli. Rales (crackles) would be heard. Mechanical
ventilation (intubation of a pipe in the throat by a tracheostomy
to help with gas exchange) is needed. The pulmonary oedema
would increase respiration rate and deteriorate the already
compromised gas exchange, leading to respiratory failure. Listen
to the crackling sound.
3. In the heart, the cells for the electrical system die, causing
dysrhythmia and the cells, which consist of myocardium die,
leading to a myocardial infarction and decreased inotropic effect
—eventually HF.
4. In the kidneys, the cells, which consist of nephrons, die and cause
acute tubular necrosis and kidney failure. So, the BUN (5-20) and
 creatine (0.6-1.2) will go up, and urinary output will go down
(oliguria, 30ml/hr-more accurately, 0.5-1.5ml/kg/hr). The amount
of blood metabolic waste will increase, leading to metabolic
acidosis and coma.
5. In the GI, the cells consisting of the intestinal lining die, leading to
massive GI bleeding (as the liver is not making the clotting factors
due to lack of o2).
6. In the liver, cells death led to liver failure. The risk of infection
would increase. The amount of bilirubin will increase (<1, RBC
recycle byproduct, jaundice), and the ammonia will increase (15-
45, protein digestion byproduct), which leads to coma. Less
clotting factor being made causes haemorrhage (the GI) and DIC.
also signs of infection shows
7. Dissemination intravascular coagulation (similar to heparin-
induced thrombocytopenia) will form micro clots in the vessels,
and these tiny clots would block the blood supply to organs and
deplete platelets. The depletion would deteriorate the
haemorrhage. Monitor IV sites bleeding.

The refractory stage is unreversible, anuria, and multiple organ

dysfunction syndrome will deteriorate the existing issues and die.
During MODS, level of consciousness, UOP, peripheral pulse/sensation,
skin colouration, and extremities temperature are used to access tissue
perfusion. Clinical MODs manifestations are acute respiratory distress
syndrome (low respiratory compliance/chest expansion), kidney
function (aliguria/BUN/creatine/fixed urine gravity), decreased albumin
and prealbumin, coma, myocardial dysfunction, and DIC.

In an emergency, nurses should follow airway/breathing/circulation

(ABC). So administrate o2 first. Then cardiac monitoring and 2 IV access
in antecubital fossa for fluid resuscitation, administrating meds, and
blood culture. Giving sympathomimetic drugs like a vasopressor if fluid
replacement failed to maintain MAP>65. Vasopressors like vasopressin
can cause extravasation in the antecubital fossa, manifested as
coldness and pallor at the infusion site. The leakage of the vasopressor
causes local vasoconstriction and increases the risk of necrosis and limb
amputation. Stop STAT and swap to centreline (not the first choice as
using centreline increases the risk of infection and DVT) when
extravasation happens. Usually keeps the head flat.
Cardiogenic shock (has nothing to do with the blood volume)

Cardiac output = 4-8L/min = HR* stroke volume (50-100ml/beat). Meds

can alter stroke volume to increase contractility (digoxin) and decrease
pre/afterload (vasodilators like nitroglycerin or sodium nitroprusside).

The cardiac index is an assessment of cardiac output and tissue

perfusion. The average cardiac index is 2.5-4l/min/m2. CI
<2.2/min/square meter and narrow pulse pressure presents (systolic-
diastolic pressure=pulse pressure< 25% of systolic pressure) when
having cardiogenic shock.

Cardiogenic shock happens when the heart has issues with systole or
diastole. MI is the main cause of cardiogenic shock. Then pericardial
tamponade (diastolic issue) is followed, which refers to
pericarditis/fluid accumulation (by aortic aneurysm-dissection or lung
cancer etc., But anything can change the size of the heart or lungs) in
the pericardial layers putting pressure (squeeze) against heart diastole.
Also, arrhythmia, carditis, and valve stenosis.

During the cardiogenic shock

A decreased cardiac output leads to fluid backflow to the lungs (rales

present). The patient would have dyspnoea, orthopnoea, increased RR
(<38 paco2)/HR/pulmonary capillary wedge pressure (>18, normally 8-
12), and then the fluid backflow to the right side of the heart, causing
an increased central venous pressure leading to jugular vein distension.
Meanwhile, the patient would experience decreased BP, <60MAP, and
cardiac index (<2.2), leading to cell hypoxic injury, hypotension and
diminished peripheral pulse and cold skin (now blood is reallocated to
the heart and brain and capillary refill>2s). The cells consist of AV nodes
and myocardium dies leading to arrythmia and myocardial infraction.

In the kidney (main organ for ph balance), a decreased blood supply

triggers RAAS to release angiotensin 2. Angiotensin 2 will directly cause
vasoconstriction. Angiotensin 2 stimulates the adrenal gland to release
aldosterone for keeping sodium and therefore water. Angiotensin 2
stimulates the pituitary gland to release antidiuretic hormone to retain
water. Therefore, the oliguria happens (UOP<30ML/hr). If the
compensation fails, the cell hypoxic injury leads to acute tubular
necrosis. So, the amount of metabolic wastes (serum lactate>4,
normally 1) and acids (<ph7.35) will increase (hitting the brain cause
coma). Also, the BUN and creatinine increases.

In the lungs, less tissue perfusion causes fewer parts of the lungs for gas
exchange. Pulmonary fluid retention in the interstitial space will
pressure the alveoli (haemoptysis) and make breathing even more
laboured.
In the liver, due to cell hypoxic injury, the amount of ammonia (protein
digestion byproduct) will increase and hit the brain, cause coma.
+bilirubin (jaundice)

In the brain, acidosis, less perfusion, and ammonia will deteriorate the
mental status (agitation) and eventually cause no reaction to
stimulations (coma).

Nursing intervention

Put patient in semi-Fowler's position (body position at 30° head-of-

bed elevation), Preparing IV/centreline (using centreline is not the first
choice as it increases the risk of infection) access, maintaining
oxygenation, nasal cannula/mask/mechanical ventilation (intubation),
urinary catheter insertion to monitor UOP (>30ml/hr), monitoring signs
of increased tissue perfusion such as normal RR/HR/BP, skin warmness,
capillary refill<2s, UOP>30ml/hr. Monitor signs of fluid overload like
jugular vein distention or rales. Monitoring troponin (<0.8, shows after
2-4hrs of MI, draw every 4 hrs), BNP (<100, signs of HF when the
ventricles are overstretched), creatinine, BUN, blood gas (ph>7.35,
serum lactate<4), high ALT/AST ratio, bilirubin (<1), ammonia (<45).
Platelets (>15000), chest x-ray for pulmonary edema, echocardiogram
for ejection fraction (50-75%, <40 during HF), CVP <12, PCWP <18
(normally 4-12). The PCWP in normal range is the best indicator for the
effectiveness of the treatment. Then warn/pink skin. An increased BP
and HR and decreased troponin numbers are not necessarily indicate
better tissue perfusion. A decreased troponin is not an indicator for
tissue perfusion.

Meds for cardiogenic shock

Diuretics against pulmonary oedema by MI or lower the blood volume

to decrease with cardiac workload and o2 demand and pulmonary
oedema like frusemide (10 mins onset), but watch for hypokalaemia
(<3.5, digoxin toxicity 0.5-2), hypomagnesemia (<2.5), hyponatremia
(<135, lithium 0.5-1.2), hyperglycaemia (>70-100/7.8), and
hyperuricaemia (>7/42). Administrate loop diuretics slowly or
ototoxicity.

Sympathomimetic drugs like vasopressors like

noradrenaline/vasopressin (risk of cardiac ischemia) cause
vasoconstriction (MAP>60) and improve tissue perfusion. Dobutamine
has inotropic effects but causes hypotension/hypokalemia. Dopamine
(cant be mixed by bicarbonate or aminophylline solution)has inotropic
effects/vasoconstriction but can cause tachycardia. No phenylephrine
in cardiogenic shock. Giving a vasopressor via IV can cause
extravasation manifested as coldness and pallor at the injection site.
The leaked vasopressor cause localised vasoconstriction, necrosis, and
amputation. Stop vasopressor STAT and swap to centreline (increased
risk of infection).

Vasodilators like nitroglycerin or sodium nitroprusside (arteriole

vasodilator) can decrease the preload and afterload (high SVR), so less
workload/oxygen demand for the heart but watch for hypotension.

Ventricular assist devices like an intra-aortic balloon pump deflates

when systole and inflates when diastole to increase the cardiac output.
Hypovolemic shock

Patients would show the S&S of hypovolemic shock after they lose 15%
(750ml) of their blood (average 5L).

In relative hypovolemic shock (concealed internal haemorrhage), fluid

moves from the intravascular space to the interstitial space. Causes are
bone fractures, severe burn (concurrent with increased capillary
permeability), acute pancreatitis (signs are Cullen sign- hematoma
around umbilicus and Turner sign- hematoma in flanks.), and
septicaemia (excessive vasodilation and high capillary permiability).

In absolute hypovolemic shock, fluid moves from intravascular space to

the outside of the body. Causes are haemorrhage (injury/surgery) or
excessive fluid loss like hyperemesis, explosive diarrhoea, polyuria, and
hyperhidrosis (these symptoms are related to endocrine disorders like
diabetes).

Pathophysiology

Decreased venous return-decreased preload-decreased stroke volume

(<50-100ml/beat)-decreased cardiac output/index (<2.2) (=stroke
volume * HR=4-8L/min). Also widen pressure presents (systolic-
diastolic=pulse which>60)-less perfusion- cells swap from aerobic
metabolism to anaerobic metabolism- potentially acidosis (blood gas
shows normal serum lactate 1, >4 in acidosis, ph<7.35, coma).
In class 1, <15%, <750ml-initial stage

Every vital sign is within the normal range. UOP>30ml/hr

(0.5-1.5/kg/hr), warm skin, and capillary refill within 2s.

In class 2, 15-30%, 750-1500ml-compensatory stage.

1. Tachycardia (<120) occurs as the baroreceptors in the aortic arch

and ocarotid sinus detects the lowered BP, and the baroreceptors
stimulate SNS to release
adrenaline(bronchodilation)/noradrenaline (vasoconstriction) to
increase the inotropic/chronotropic/BSL.
2. BP increased but within normal ranges. The noradrenaline and
angiotensin 2 cause vasoconstriction.
3. Oliguria (less than 30ml/hr) as the inadequate renal perfusion
triggers RAAS and aldosterone (adrenal glands) makes the renal
system keeps sodium, and ADH makes the renal system keep the
water and vasoconstriction. Additionally, the body will allocate
fluid from the interstitial space to the intravascular space.
4. Skin-cold as blood now is allocated to the brain and heart (listen if
bowel sounds are absent due to paralytic ileum). Capillary refill
>2s. Diminished pulse
5. Increased RR as fewer parts of the lungs are functioning (<38
paco2).
In class 3, 30-40%, 1500-2000ml-progressing stage, cells start to die and
necrosis.

1. RR increases as the acute respiratory distress syndrome happen.

Pulmonary oedema happens as the increased capillary
permeability moves fluid from the intravascular space to
interstitial space and squeezes the alveoli to expand. This
pressure, plus the already less functioning respiratory system, will
cause laboured breathing and increased RR. Also could cause
cardiac tamponade (the size of the lungs increased) and diastolic
dysfunction. Rales present. Mechanical ventilation by intubation
via tracheostomy is needed.
2. Tachycardia (>120)
3. Hypotension and diminished pulse. Now the mean arterial
pressure will be less than 60 (normally 70-110) as less blood
returned. The central venous pressure will be less than 8 (8-12),
and the pulmonary capillary wedge pressure will be less than 4 (4-
12).
4. Oliguria and renal failure. Cell death leads to acute tubular
necrosis. It is indicated as metabolic wastes (ph), BUN and
creatine increase drastically.
 5. Bleeding internally as the liver will not make clotting factors/ DIC/
and the lining cells of GL die and gastric acid hits the GI. High
ALT/AST ratio. Bleeding externally (IV sites?)
6. Mental status deteriorates. An excessive amount of ammonia hits
the brain, acidosis (serum lactate >4) and low MAP (<60), leading
to anxiety/confusion.

In class 4, >40%, 2000ml-refractory stage

1. Significant tachycardia (>140), increased RR, severe hypotension,

anuria, coma, and bye.

In a nutshell, +HR, RR capillary refill time,-UOP, BP, widen pulse

pressure (systolic-diastolic=pulse pressure which >60), integumentary
temperature, mental status.

Nursing intervention for hypovolemic shock

1. Catheter insertion to precisely monitor UOP (anuria or oliguria

unwanted. Should be >30ml/hr or 0.5-1.5ml/kg/hr)
2. Oxygenation (nasal cannula/oxygen mask/mechanical
ventilation/intubation).
3. Monitor haemodynamic statuses and vital signs like ideally
MAP>70, PCWP >4. CVP >8, BP, HR, RR, capillary refill, skin
temperature (blood allocation), and mental status.
4. Press the wound if bleeding.
 5. Put the patients in a modified Trendelenburg position (body
straight and legs up) to help with venous return (supine, body flat
and leg elevated by 45 degrees, opposite to semi flower position).
6. Obtain at least two IV sites, at least 18 gauge for the large veins.
7. Collecting blood results like haemoglobin count, haematocrit
(blood/haemoglobin ratio, usually around 45%, to see if the
patient needs blood products), platelets count (>150000), BUN (5-
20), creatine (0.6-1.2), ALT/AST ratio, ammonia (15-45), bilirubin
(<1), blood gas such as serum lactate (>4 when acidosis) and ph
(7.35-7.45), ejection fraction (50-75%)

Fluid for hypovolemic shock. The cardiac output would be increased

with fluid resuscitation.

Crystalloids- normal saline/plasmalyte/ lactated ringers are the most

commonly used fluid. Crystalloids need to be warmed up before giving
to prevent hypothermia which interferes with clotting factors.
Crystalloids are given in 1: 3 ratios, like 1500ml blood loss, giving
4500mls crystalloids to compensate. However, crystalloids can cross
vessels (more than colloids) into interstitial space and therefore need to
watch for fluid overload. If the overload happens, the CVP and PCWP
(>12/18, cardiogenic shock) will go up, rales/dyspnoea will present, and
oedema will show (jugular vein distension, gained girth, legs).
Colloids- albumin/hetastarch- have larger molecules that cannot diffuse
into the interstitial space. Therefore, colloids would stay in the
intravascular space longer than crystalloids to maintain the cardiac
output. Colloids need to be warmed up before giving to prevent
hypothermia which interferes with clotting factors. However, colloids
have a risk of anaphylaxis and also need to monitor fluid overload
symptoms like increased CVP/PCWP (>12/18), rales, and oedema
(jugular distension/legs/girth etc.).

Blood products- packed RBCs/platelets/fresh frozen plasma. PRBCS

gives extra haemoglobin, so more o2 would be delivered to cells
(hematocrit/haemoglobin count) than crystalloids and colloids.
Platelets help with clotting, and FFP increases clotting factors. All the
blood products need to be monitored for transfusion reactions.
Neurogenic shock/vasogenic shock (a type of distributive shock)

Neurogenic shock is caused by spinal injury (above T6,

thoracic/cervical), spinal analgesia, and drugs that damage SNS (a part
of the autonomic system). SNS control the vasomotor tone (vessel
diameter) and HR by releasing adrenaline/noradrenaline/RAAS
(adrenaline/noradrenaline combine with beta 2 receptors of JG cells
then release renins). The damage of SNS causes nothing to oppose the
PSNS and therefore PSNS being dominant and causes S&S like:

1. Hypotension/low SVR. When SNS is not working, and PSNS is

dominant, no adrenaline/noradrenaline is released. Therefore,
excessive vasodilation and less venous return (risk of DVT, low
CVP<4/PCWP <8) happen.
2. Bradycardia happens when no SNS and adrenaline/noradrenaline
is released against PSNS effects.
3. Hypothermia. Blood is not returning to the heart, causing
warm/dry extremities, but the core is hypothermic.
4. Absence of Babinski’s reflex (feet tickle)
5. Full balder due to automatic dysreflexia.

Nursing interventions
1. Maintain the airway/breathing using nasal
cannula/mask/mechanical ventilation (intubation).
2. Maintain the MAP >85 for tissue perfusion by using crystalloids
cautiously, as fluid resuscitation can easily cause fluid overload
(the total body fluid is still 5L during neurogenic shock). Warm the
fluid up before giving to prevent hypothermia, which interfere
with clotting factors. Watch for dyspnoea, oedema, increased
CVP/PCWP and listen if rales are present. If not working, use
dopamine (cant be mixed by bicarbonate or aminophylline
solution)/phenylephrine to increase the HR/positive inotropic
effects and vasoconstriction (not dobutamine as it worsens the
hypotension). Watch for fluid extravasation (the vasopressor leaks
from the antecubital fossa vein causing local vasoconstriction and
necrosis. Risk of amputation and need to stop the vasopressor
STAT). Also, using atropine increases the HR by blocking PSNS
effects (decrease vagal stimulation). At last, a temporary
pacemaker can be inserted to maintain the heart rhythm.
3. Keep the environment warm. Patients with neurogenic shock are
prone to hypothermia.
4. No leg crossing or placing a pillow under the Knees as they could
compromise the circulation (DVT).
5. Catheter insertion to monitor UOP (>30ML/HR).
6. Applying sequential compression device/pressure
stockings/heparin/warfarin/claxane to prevent DVT.
7. Keep the spine immobilised, backboard, log rolling.
Anaphylactic shock

Allergens include:

food like shellfish/peanuts/dairy products or

medications like contrast dye/vaccine/NSAIDs/antibiotics or

others like latex/venom

enter the body via injection (parenteral)/inhalation/oral (enteral)/skin

causing anaphylactic shock.

In anaphylactic (immune/IgE involved) reactions (type 1), the shock

doesn't happen during the first exposure. After the allergens enter the
body, immunoglobulin E (IgE), a type of antibody, is made and binds
with the mast cells and basophils for the next time exposures, and now
the person is sensitized. In the subsequent exposure, the allergens will
attach to the IgEs (works like plug and socket), and the leukocytes (mast
cells/basophils) will release histamines.

In anaphylactoid reactions, the shock happens during the first

exposure. No sensitization/IgEs are involved. Allergens can directly
activate mast cells and basophils and cause the release of histamines.

When histamines are released, it causes vasodilation (DVT,

hypotension), so BP/tissue perfusion drops. Fever when the shock
presents.
  Histamines increase capillary permeability, so fluids move from
intravascular to interstitial space. So BP/tissue perfusion drops,
and edemas show (+extremities/girth/bronchospasm/upper
airway swelling, rales).
 Histamines cause
bronchoconstriction/bronchospasm-dyspnea/wheezing-
respiratory failure.
 Histamines cause tachycardia.
 Histamines increase gastric secretion/peristalsis leading to
pain/N+V/diarrhea, H2 helps with gastrointestinal symptoms.
 Histamines cause itchiness or angioedema on the skin.

Nursing intervention

Clean the allergen, this is the FIRST (e.g., stop the allergy-causing
medication) and maintain the airway by nasal
cannula/mask/mechanical ventilation. STAT CPR if necessary.
Monitoring the vitals. Putting the patient in modified Trendelenburg
position (body straight head low legs high) to increase venous return
unless the patient is vomiting or airway swallowing that could cause
suffocation. Keep monitoring the patient's S&S of the anaphylaxis due
to the risk of biphasic anaphylaxis. Biphasic anaphylaxis refers to the
second anaphylaxis that could happen without triggering, ranging from
a few hours to 72 hours after the first anaphylaxis.

Administering adrenaline (no IM form for noradrenaline) in IM or IV (if

in a hospital setting). Adrenaline causes vasoconstriction/alleviates
bronchoconstriction (the main reason)/decreased capillary permeability
to increase venous return. Adrenaline causes bronchodilation/positive
inotropic/chronotropic to alleviate chest tightness. Only giving epi-pen
on the middle of the outer thigh (NOT ABDOMEN), the pen can
puncture through clothes, inject and hold in place for 3s, and massage
the injection site for 10s.

Fluids can be given (warming up to prevent hypothermia which hinders

clotting factors) in 1-2L (no fluid loss in the scenario) to increase the
venous return but watch for fluid overloads like CVP/PCWP >12/18,
rales, dyspnea, and edemas. Albuterol cause bronchodilation (similar to
budesonide/Symbicort but budesonide for daily symptoms control and
albuterol for resuscitation only). H1 antihistamines like
diphenhydramine (similar to promethazine) inhibit anaphylactic
symptoms. H2, like famotidine/ranitidine/omeprazole, only works on
reducing gastric acid. Corticosteroids are given to prevent future
inflammation/biphasic anaphylaxis (slow onset like your budesonide).
Spo2 is the gold criteria to measure the treatment effectiveness
because the airway odema is the way to first kill.
Septic shock

Microorganisms like bacteria, which is the most common cause of

sepsis, gram-positive/negative, virus, parasite, or fungus, enter the
body, causing an infection (pneumonia/UI infection/cellulitis/blood
infection) and trigger hyperactive systematic immune responses by
WBCs releasing cytokines that produce nitric oxide.

nitric oxide causes hypotension and insufficient tissue perfusion by

1. Vasodilation (to increase WBCs presence)

2. Increase capillary permeability (WBCs can travel to the infectious

tissue but cause low tissue perfusion)

3. Making heaps of clots and depleting platelets to patch the sites

damaged by WBCs. Later cause the dissemination intravascular
coagulation and less tissue perfusion (the clots will block the vessels
systematically). Bleeding/oozing.

4. lower EF (only at the progressive stage)

2 or more out of 4 systemic inflammatory response syndromes equal

SIRS criteria.

 >38 and <36/<97 and 99>

  Tachycardia
 >20RR, paco2 <32 low when hyperventilation so co2 goes out the
body. (38-42 normally)
 WBC count >12000 or <4000 (4500-11000 normally) or >10% band
cells (immature leukocytes are released in an emergency to
against the inflammation). WBC goes high as the response to the
inflammation and low when the inflammation overwhelms.

Sepsis= SIRS+ a confirmed infection

Septic shock = characters of septic shock + sepsis

 Persistent hypotension with ongoing fluid resuscitation. The

refractory hypotension is caused by massive vasodilation (DVT-
pool/stasis) and increased capillary permeability
(hypovolemia/relative hypovolemic shock).
 MAP<65 (70-110) without vasopressors (NE is the first line or
noradrenaline + dobutamine)
 Serum lactate >2 (<1 normally)
 An infection presents
 Two of four systemic inflammatory response syndrome (SIRS)
criteria
Vulnerable people are

 Suppressed immune systems (antiviral

therapy/chemotherapy/immunosuppressive therapy-organ
transplant/steroids/malnutrition) - they are prone to infections
and should be on isolation to lower the risk.
 Elderly
 People with organ transplants (immunosuppressive therapy)
 Surgical procedures (microorganisms enter the body)
 Indwelling devices (catheter, centrelines, intubation-mechanical
ventilation gives access for microorganisms to enter)
 Sickness (chronic inflammation, e.g., UI infection, pneumonia, DM
(prone to another infection and hard to heal), cirrhosis, hepatitis,)
 malnutrition

S&S in the compensatory stage (warm phase)

 Warm skin due to vasodilation

 Hyperthermia and lethargy (immune system working)
 Hyperdynamic circulation= abnormally high cardiac output but
low CVP/tachycardia/tachypnoea (RR>20, Paco2<32). The heart
 and lungs are compensating for the decreased venous return and
hypotension caused by vasodilation and increased capillary
permeability.
 Decreased BP and SVR (vasodilation/permeability)

S&S in the progressive stage (cold phase)

 Hypothermia
 Severe/refractory hypotension due to massive vasodilation and
permeability.
 Tachycardia
 Decreased cardiac output and EF
 Oliguria
 Coma

Treatment sequence is oxygenation, preparing IV sites, fluid

resuscitation, administering vasopressor if hypotension still presents,
obtaining blood/urine culture, administering antibiotics and other
meds.

Treatment goals are

 Maintain tissue perfusion (MAP>65). Firstly, using fluid

resuscitation. Preparing at least 2 IV sites, warm the fluids up
 before giving to prevent hypothermia which interferes with
clotting factors. Watch the signs for fluid overload (more likely
crystalloids-normal sealine/plasmalyte), such as
rales/dyspnoea/CVP>8, PCWP>18/jugular vein
distention/oedema. Watch for anaphylactic signs (colloids only-
hetastarch/albumin) such as airway swelling/itchiness/dyspnoea/.
Applying haemodynamic. Ideally, CVP 8-12 and PWCP 4-12. If the
fluid placement is not working (usually CVP increased but not BP),
then use sympathomimetic drugs like vasopressors.
Noradrenaline (only IV forms available) is the first choice, then
noradrenaline + dobutamine. Dobutamine stimulates beta 1 for
inotropic effects and vasodilation (which is counteracted by
noradrenaline). Then phenylephrine. Watch for extravasation and
ischemia at the infusion site surrounding when giving
vasopressors. The leaking sign of vasopressor is coldness and
pallor at the infusion site. Extravasation causes local
vasoconstriction and then necrosis and amputation. Stop STAT
and swap to centreline (although it increases the risk of infection).
Using vasopressin (increase the risk of cardiac ischemia) when
MAP is stable can lower the catecholamine dependence.
 Against infection is the priority (within 1hr of the shock starting).
Firstly performing blood or urine culture to identify the bacteria,
 then using broad spectrum antibiotics and later using the specific
antibiotics after the blood or urine culture results.
 Catheter insertion to monitor UOP (>30ml/hr)
 Maintain oxygenation >95% by nasal cannula/oxygen
mask/mechanical ventilation (intubation by
tracheostomy/endotracheal tube) to against acute respiratory
distress syndrome.
 Decrease inflammation by using corticosteroids which also
enhance the effectiveness of noradrenaline and cardiac function.
 Control BSL (goal is lower than 180) as hyperglycaemia hinds
immune function. Patients without DM can have hyperglycaemia
during septic shock.
 Provide aggressive eternal nutrition to assist the immune system
functioning and giving h2 antihistamine like famotidine,
omeprazole, or ranitidine (prophylaxis) to prevent stress ulcers
(physical stress cause acidosis and damage gastrointestinal linings.
The ulcer stress would use more platelets and worsens the
hypovolemia. Monitor stool see if theres melena (blood)
Arrhythmia

Arrhythmia is an issue of heart rhythm caused by abnormal electrical

impulses. It can be bradycardia, tachycardia, or irregular heartbeat.
Supraventricular tachycardia includes atrial fibrillation (300-600), atrial
flutter (300-600) and paroxysmal supraventricular tachycardia (100-
250). Supraventricular tachycardia is usually concurrent with
MI/HTN/valve stenosis. In Atrial fibrillation (most common), the atria
beat irregularly and rapidly. In atrial flutter, the atria beat regularly and
rapidly. Atrial flutter may cause atrial fibrillation. Blood pooling can
occur as the atria are quivering and unable to empty blood. The main
leading issue of supraventricular tachycardia is thrombosis (from >48
hrs of the onset), leading to stroke/MI/pulmonary embolism etc. (Atrial
fibrillation has a higher morbidity of thrombosis) and HF as the atria are
overworked. No P wave and R-R interval are irregular in Atrial
fibrillation. The three types of Atrial fibrillation, are Paroxysmal Atrial
fibrillation (self-terminates within seven days), persistent atrial
fibrillation (>7 days), and permanent Atrial fibrillation (does not self-
terminate).
S&S are palpitations/diminished pulse/SOB/hypotension/dizziness/
tachycardia that cause bad diastole/ fatigue. They are all related to
quivering caused low tissue perfusion.

Diagnoses are 12-lead ECG and Holter monitor, a portable ECG that
provides a constant and more accurate reading of heart rhythm than
12-lead ECG.

Treatments are

Rate control medications are the primary approach in most cases.

Administering medications have negative chronotropic effects.
Selective beta-blockers like metoprolol cause negative
inotropic/chronotropic effects (by blocking the effects of
adrenaline/noradrenaline). Heart calcium channel blockers, like
diltiazem and verapamil, cause negative inotropic/chronotropic effects.
Digoxin causes negative chronotropic and positive inotropic effects.
Watch for bradycardia, HF, hypotension, angioedema (rales) and
digoxin toxicity when used concurrently with loop/thiazide
diuretics/CCB/amiodarone, manifested as N+V, halos.

Anticoagulants like warfarin/phenindione are used for Atrial fibrillation

patients with valve stenosis. Direct oral anticoagulants (DOACs) such as
dabigratran, apixaban, rivaroxaban, and edoxaban are used for Atrial
fibrillation patients without valve stenosis. Watch for signs of bleeding
such as haematemesis, haematuria, haemoptysis, melena, severe
headache (intracranial haemorrhage), and hypotension (relative
haemorrhage).

Rhythm control meds are

amiodarone (+digoxin toxicity+ extra INR with warfarin, risk of

lung/liver toxicity, and easily cause sunburn), Flecainide increases the
risk of hypotension, and sotalol (COPD/asthma). Adenosine is only for
paroxysmal supraventricular tachycardia given by rapid intravenous
bolus injection. Lidocaine is used for ventricular tachycardia and
ventricular fibrillation.

Implanted cardioverter defibrillator or radiofrequency catheter ablation

(using a laser to burn some parts of the electrical conduction system to
stabilize the pulse), and then planting a pacemaker to maintain the
rhythm of the heart.

Cardioversion is a low voltage shock used to correct rhythm.

Defibrillation (removing the oxygen mask) is used when the heart stops
with a stronger voltage.

Carotid sinus massage or Valsalva maneuver (deep breath then pinch

nose and mouth closed and breathe out) stimulates the vagus nerve
and lowers heart rate.
Ventricular tachycardia (>200, regular) is a medical emergency with
regular and rapid ventricular contractions. VT = 3PVC + 100HR. During
an emergency, apply cardioversion first; if it does not work, use
lidocaine and amiodarone and repeat cardioversion. Educate the
patient to inhale deeply and cough forcefully every 1 to 3 seconds,
which may help to terminate the tachycardia and maintain cerebral and
coronary circulation. Use defibrillation straight away if the patient is
pulseless. Patients with non-sustained ventricular tachycardia should
not be given beta blockers. Patients with sustained ventricular
tachycardia are eligible for implanting a cardioverter defibrillator
(pacemaker) and can be treated with beta-blockers, amiodarone, and
lidocaine.

Ventricular fibrillation (350-500, irregular) develops from ventricular

tachycardia and is worse because no blood circulation occurs.
Ventricular fibrillation is a medical emergency. Use STAT defibrillation,
cardiopulmonary resuscitation, red trolley, and amiodarone.
Anaemia

Anaemia refers to a decrease in the number of red blood cells (RBCs)

(4.3-6 x 10^12/L), hemoglobin (Hb) (130-175 g/dL), and hematocrit
(HCT) (35-45%). The most common type of anemia is iron deficiency
anemia, which is caused by low iron levels (60-170 ng/dL) in the body.
Hemoglobin is made from iron, and hemoglobin is a component of RBCs
that transport oxygen and carbon dioxide. When a person has iron
deficiency anemia, their Hb level is below 130-175 g/dL, leading to
reduced blood flow to the tissues. This can cause symptoms such as
fatigue, pale skin, shortness of breath (SOB), inflammation or soreness
of the tongue (glossitis), spoon-shaped nails (koilonychias), and an
increased heart rate (HR) and respiratory rate (RR) as compensatory
responses. These symptoms are caused by low oxygen levels in the
blood, which may not be evident from the oxygen saturation levels
(SPO2), and may not be noticeable in the early stages of the condition.
Some individuals may also experience cravings for unusual substances,
such as ice or clay.

The causes of iron deficiency anemia include:

 Poor iron intake in the diet, particularly in young children (1-3

years), adolescents (10-19 years), vegetarians, or during
pregnancy, when the fetus absorbs a large amount of iron, leading
 to iron deficiency in the mother. Good sources of iron include
meat, nuts, legumes, and egg yolks.
 Blood loss from sources such as menstruation, gastrointestinal
bleeding, or ulcers.
 Difficulty in absorbing iron due to intestinal surgery, as the small
intestine is responsible for absorbing most of the iron.

Diagnosis of iron deficiency anemia is made through a complete blood

count (CBC), which measures RBCs (4.3-6 x 10^12/L), hematocrit (35-
45%), hemoglobin (130-175 g/dL), platelets (150-400 x 10^9/L), iron
levels (60-170 ng/dL), and a blood smear test. The blood smear test
examines the shape and size of RBCs, and may show pale and small
cells (hypochromic and microcytic). Other tests that may be performed
include the mean corpuscular volume (MCV), which may be decreased,
and the ferritin test, which measures the amount of iron stored in the
body and is useful for early detection of anemia.

Iron supplements can be taken to increase iron levels in the body. It is

recommended to take iron supplements on an empty stomach to
enhance absorption, and taking them with vitamin C can further
enhance absorption. Taking supplements with fluid can prevent
staining. Foods that are high in iron, such as oranges and dark green
leafy vegetables, can also help increase iron absorption. However, it is
best to avoid taking iron supplements with dairy products or calcium, as
these can interfere with iron absorption. Taking iron supplements may
cause the stools to turn black (not melena or tarry stools), and may also
cause constipation.
RAAS- renin angiotensin- aldosterone- system
1. Ultimately the goal of RAAS is to increase the stroke volume, BP.
2. When BP drops, stimulates sympathetic nervous system
stimulates juxtaglomerular (JG) cells in the kidneys to produce
renin.
3. Renin breaks angiotensinogen, which is made by kidneys, into
angiotensin
4. ACE (angiotensin-converting enzyme) in the surface of
kidneys/lungs endothelium (thin membrane inside of vessels)
converts angiotensin one into angiotensin 2.
5. Angiotensin 2 attaches to angiotensin 2 receptors in the smooth
muscle of the vessels and leads to vasoconstriction. Angiotensin 2
directly stimulates the kidneys to keep sodium (h2o always
follows sodium) to increase blood volume. Angiotensin 2
stimulates the adrenal cortex to produce aldosterone. The
hormone stimulates the kidneys to keep sodium and lower the
potassium level (which causes more sodium levels in the blood).
Angiotensin 2 stimulates the pituitary gland to produce
antidiuretic hormones (ADH, vasopressin) to cause the kidneys to
keep h2o. The three approaches increase the blood volume to
increase BP.
6. That’s how ACE inhibitors work. Angiotensin 1 cannot be
converted into angiotensin 2 with less ACE. Thus no vessel
constriction, no aldosterone by produced by adrenal cortex and
no ADH produced by pituitary gland and thus less sodium and
blood volume and the BP would be lower.
Glossaries

Adrenaline/noradrenaline=both increase BSL/inotropic/chronotropic.

Adrenaline bronchodilation, noradrenaline vasoconstriction

Afterload 心脏射血力

Agitation-angrey, anxiety-fear

Angiogram-angiography-check if the patient is allergic to iodine or

shellfish to prevent anaphylactic reactions

B type natriuretic peptide (BNP) is the biomarker of heart failure when

the heart is taking excessive pressure.

Baroreceptors regulates BP by detecting BP. Chemoreceptors regulates

BP by detecting o2 level.

Both adrenaline and noradrenaline increase HR/BSL/contractility.

Adrenaline relaxes smooth muscle in airways to assist breathing and
noradrenaline constricts the smooth muscle around vessels for
vasoconstriction.

Catecholamine is an umbrella term for dopamine, adrenaline, and

noradrenaline.

3 types of ecgs are 12 leads ecg/cardiac stress ecg(trademill ecg)/holter

monitor (portable ecg)
Central venous pressure (usually monitored in ICE) detects cardiac
preload and used to monitor fluid volume status. Normal CVP 8-12. CVP
is high during cardiogenic (bloods moves back from L to R) and low in
hypovolemic shock (less fluid available)

Ejection fraction is the precentage of blood being ejected by the left

ventricle (usually 50-75%). Low EF=HF=high CVP.

Extravascular=interstitial

Normal HR <130<90. High HR 140<, 90<

Oliguria-polyuria

Orthostatic hypotension means bp is not maintained during position

changing. Orthostatic hypotension refers to 10-15 drop of systemic
pressure and 10%-20% increase in HR.

Pharmacodynamics- how body reacts to the drug

Pharmacokinetics- abosrption/distribution/metabolism/elimination

Preload is the volume of left ventricle when stretching.

Preload-射血前的装载量

Pulmonary capillry wedge pressure usually 4-12. PCWP=PAWP=PWP.

Low PCWP= hypovolemic shock. High PWCP= left ventricular failure or
mitral stenosis/pulmonary odema (PCWP increases as fluid can't be
ejected or stuck due to valve stenosis). Odema+normal PCWP= acute
respiratory distress syndrome/non cardiogenic odema.

Pulse pressure= systolic – diastolic pressure.

Spine- c1-7, t1-12, l1-5

Pulse pressure=systolic-diastolic pressure

Widen pressure= systolic-diastolic pressure>60, presents in

hypovolemic shock.

Narrow pulse pressure= pulse pressure < 25% of systolic pressure,

presents in cardiogenic shock.

supraventricular tachycardia means when atrium beats abnormally fast

when electrical impulse is disrupted. Atrial fibrillation or atrial flatter is
a type of supraventricular tachycardia when atrium beats irregularly
and rapidly.

Thrombolytic-thrombus busting, thrombotic=thrombosis- clotting,

antiplatelet-prevent platelets aggregation, arteriosclerosis- the artery
become stiff, arthrosclerosis- a type of arteriosclerosis, platelets
building up, thrombus- a plaque raptures and a clot forms, thrombosis-
the formation process of a clot reduces blood circulation. Embolism- a
clot or an object stuck somewhere in a vessel and reduce blood
circulation. Thromboembolism- clot stuck somewhere in a vessel and
reduce blood circulation

Cardiopulmonary resuscitation=CPR

MOBILE CARDIAC Telemetry is an PORTABLE observation tool that

allows continuous ECG (4 leads), RR, SpO2 monitoring up to 30 days
Medications for cardiovascular diseases:

ACE (angiotensin-converting enzyme) inhibitors

ACE inhibitors indications:

1. ACE inhibitors are indicated for HTN (against RAAS). ACE inhibitors
work on the RAAS by stopping converting angiotensin 1 to
angiotensin 2 to avoid vasoconstriction, less antidiuretic hormone,
and less aldosterone produced by the adrenal cortex to lower the
BP. So less na+ and more K+ (could cause hyperkalemia). ACE
inactivates bradykinin, and bradykinin causes vasodilation (So not
for asthma/COPD). On the other hand, because bradykinin is an
inflammatory substance, it triggers dry coughs. ACE inhibitors
hamper the process of bradykinin inactivation and dry cough as a
potential A/E.
2. When the left ventricle can't pump blood out (heart failure), ACE
inhibitors decrease the preload by vasodilation, so less blood in
the ventricles is pumped and, therefore, less workload for the
ventricles. ACE inhibitors also decrease the afterload by
vasodilation, so there would be less resistance (SVR) for blood to
be pumped forward. Afterload is the pressure the ventricle needs
to overcome to open the semilunar valves (the aortic and
pulmonary valves) and pump the blood out of the heart.
 3. ACEI helps with myocardial infarction as the heart works less
vigorously and consumes less oxygen (less preload, afterload).
4. Slowing down the diabetic nephropathy progress in T2DM
(deterioration of renal function). In T2DM many patients have
kidney failure and the kidneys are vigorously filtering the protein
in blood and therefore the proteins would be excreted to urine
manifested as proteinuria. ACEs slow down the diabetic
nephropathy progress in T2DM (deterioration of renal function).
by lowering the BP so less blood would go to the kidneys and less
workload, therefore.
5. ACEIs are teratogenic.

ACE inhibitors ends up pril. Like cilazapril, captopril, enalapril, lisinopril,

perindopril, ramipril, benazepril and quinapril.

Nurses' responsibility for ACEI

1. Closely monitoring BP (hypotension)/HR (arrythmia)/UOP

(>30ML/HR) as ARBs and ACEIs against RAAS. ARB/ACEI self cause
hyperkalemia (3.5-5) and the risk increases when concurrent with
potassium sparing diuretics like
amiloride/spironolactone/eplerenone.
 2. Monitoring renal failure. For patients who have heart failure, their
renal blood supply is delicately maintained by RAAS. ARBs stop
RAAS leading to a lack of blood supply and renal failure would
happen. The renal failure is manifested by low UOP
(<30ml/H/oliguria/anuria). The fluid retention happens, and
therefore monitor daily weight is needed (3ibs/day-5ibs/week),
and elevated BUN (5-20) and creatine (0.6-1.2mg/dl)
3. Monitor liver enzyme
4. Monitor angioedema (drug induced anaphylaxis that fluid builds
up under the skin) although ACEI has a higher incidence. Checking
if there's SOB (crackle sounds ln the lungs), oedema in limbs or
face, and daily weight(3day/5week).

A/Es of ACEI

1. Persistent dry cough (normal) but big problem if the cough is SOB
caused by fluid retention (rales/angioedema).
2. Dizziness/orthostatic hypotension (low BP so move slowly)
3. Increased K+. So the nurse should watch of hyperkalemia which
could cause arrythmia. K+ should be within 3.5-5
4. Angioedema, which is an anaphylactic reaction that fluid builds up
under the skin, manifested by mostly swelling and SOB. Its 111.

Patient education
1. Take ACEIs an hour before meal (like Aspirin)
2. Asking the patient to monitor and record BP and HR regularly
3. Since RAAS stopped and less sodium and more potassium (like a
seesaw and the normal K+ should be 3.5-5meg/L) Asking the
patient to avoid salt (salt products contain potassium) and high
potassium foods like potatoes, bananas, spinach, oranges, and
pork. Especially if the patient is on potassium supplements or
potassium-sparing diuretics like spironolactone/eplerenone.
4. Even the dry cough is bad, the ACEI cannot be stopped abruptly.
the patient needs to get confirmation from the doctor because of
the rebound hypertension which is life-threatening.
5. Asking the patient to be aware of the symptoms of angiodema
like swelling or SOB. Listening to the crackle sounds means the
fluid retention in the lungs.
6. If the patient misses one dose, never double dosing which leads to
severe hypotension.
ARB: Angiotensin 2 receptor blocker. Starts with sartan. Losartan

ARBs work on RAAS. In the RAAS cycle, vasoconstriction and increased

sodium/water retention would happen when angiotensin 2 attaches to
angiotensin 2 type 1 (AT1) receptors in the smooth muscle of vessels
and the adrenal gland, ultimately increasing the BP. ARBs work by
stopping the angiotensin two attached to AT1. As the pharmacological
effects of ARBs, SVR would decrease (be aware of angioedema-fluid
builds up under the skin, hypotension, renal functions-less blood
supply.), and the levels of potassium would increase (angiotensin 2
stimulates the kidney to keep sodium. The levels of potassium and
sodium are always like a seesaw in kidneys. normally 3.5-5meg/L of
potassium and hyperkalemia would cause arrhythmia). In ACEs, with
the activation of bradykinin, bronchoconstriction would happen
(asthma). On the other hand, bradykinin is an inflammatory substance.
It could trigger dry coughs. With ARBs and the presence of angiotensin
2, the bradykinin would be inactivated and hence bronchodilation (so
ARBs are ok for COPD/asthma). ARBs are teratogenic but safer than
ACEIs.

ARBs are indicated to

1. HTN just like ACEs.

 2. ARBs Mitigate the progression of Diabetic nephropathy
(deterioration of renal function). High levels of BSL would damage
the blood cluster in the kidneys. Therefore, the proteins in the
blood would not be sufficiently filtered and are excreted into the
urine, manifested as proteinuria. Because the workload is out of
the system’s capacity, the T2DM renal system function would
deteriorate furtherly, leading to renal failure. ARBs mitigate
nephropathy progress by decreasing the workload of the kidneys
as ARBs decrease the BP/less blood flow. But CONTRAINDICATED
TO RENAL FAILURE as not enough blood supply for the patients.
3. Heart failure happens when the afterload is above the
contractility of the ventricles. The disorder causes oedema (RHF).
ARBs work the same as ACEI by decreasing mainly the afterload as
the SVR is decreased by vasodilation and preload as there is less
sodium in the kidneys. So, the blood would be pumped easier.

Nurses' responsibility for ARBs and is similar to ACEI.

1. Closely monitoring BP (hypotension)/HR (arrythmia)/UOP

(>30ML/HR) as ARBs and ACEIs against RAAS. ARB/ACEI self cause
hyperkalemia (3.5-5) and the risk increases when concurrent with
 potassium sparing diuretics like
amiloride/spironolactone/eplerenone.
2. Monitoring renal failure. For patients who have heart failure, their
renal blood supply is delicately maintained by RAAS. ARBs stop
RAAS leading to a lack of blood supply and renal failure would
happen. The renal failure is manifested by low UOP
(<30ml/H/oliguria/anuria). The fluid retention happens, and
therefore monitor daily weight is needed (3ibs/day-5ibs/week),
and elevated BUN (5-20) and creatine (0.6-1.2mg/dl)
3. Monitor liver enzyme
4. Monitor angioedema (drug induced anaphylaxis that fluid builds
up under the skin) although ACEI has a higher incidence. Checking
if there's SOB (crackle sounds ln the lungs), oedema in limbs or
face, and daily weight(3day/5week).

Patient education

1. Risk of fall as hypotension so moving slowly.

2. Regularly monitor BP and HR
3. Avoid potassium diet or spironolactone which is a diuretic and
increasing potassium levels and leading to hyperkinemia (3.5-
5meg/L) and arrythmia.
4. Never double dosing (hypotension) or stop before asking doctor
as rebound HTN can kill.
5. Lifestyle changes are needed becasue the med only alleviate.
Beta-blockers are indicated for hypertension, stable angina (reduces
the contractility and rate of the heart, thus less o2 demand),
dysrhythmia (by lowering the HR), and glaucoma (non-selective beta
blockers). Normally SNS stimulates increased HR, BP, systole
(myocardium contractility), glucose (glycogenolysis), and
bronchodilation (more o2) for fight or flight. Beta blockers against the
effects of adrenaline and noradrenaline (negative
inotropic/chronotropic effects). End with LOL is meds of beta blockers.

Selective beta-blockers only work on beta 1, more specifically on

cardiac nodal tissue (HR) and cardiac myocytes (contractility), renal for
renin producing. Selective blockers are atenolol, esmolol, and
metoprolol. Be aware of A/Es (TOO MUCH
parasympathetic/acetylcholine effects) like bradycardia (HR lower than
60, heart block) or heart failure (less contractility cause fluid stagnancy
like blood stuck in the lungs or body, noticing crackles sound) or
lowered perfusion (less sensitivity of beta 1 in the kidneys causes less
RAAS effects)

Beta 2 receptors are in the lungs, GI tract, vascular smooth muscle and
eyes (beta2 for glaucoma). Nonselective beta-blockers work on both
beta 1 and 2 receptors. Nonselective blockers are propranolol, sotalol,
and timolol. Be aware of bronchoconstriction (SOB) in patients with
asthma or COPD. Additionally, beta blockers can cause hyper but
mostly hypoglycaemia. When diabetic patients have hypoglycemia, and
it is accompanied by tachycardia, selective/non-selective beta blockers
can hide the tachycardia, so the nurse must monitor the sugar levels
closely.

Patient education:

1. The overdose effects are similar to neurogenic shock that the

parasympathetic/acetylcholine effects overwhelm.
2. Bradycardia (cardiac nodal tissue), heart block, when the electrical
impulse that triggers heart contraction is disrupted.
3. Exacerbation of heart failure (less contraction as less myocytes in
myocardium are stimulated). Monitoring the lung sound (crackles,
fluid retention), swelling, and weight gain (fluid retention)
4. Taper off (around 2 weeks) in case of the recurrence of HTN and
angina.
5. Asthma (non-selective BB blocks beta 2 receptors in the lungs
causes bronchoconstriction)
6. Blood sugar (the lowered HR masks the symptom of
hypoglycemia, tachycardia). SNS stimulates fight flight so more
 glucose supposed to be produced by glycogenesis. Beta blockers
hind the glycogenesis.
7. Lowered hypotension (beta1 receptor activation triggers the
releasing of the renin)
Digoxin belongs to the cardiac glycoside family. Digoxin indicates heart
failure, cardiogenic shock (commonly caused by MI) and Afib. They all
mean the heart is not pumping and emptying correctly. Digoxin
increases myocardium's cardiac contractility (inotropic effect) to
increase stroke volume by inhibiting the sodium and potassium pumps
in myocytes. Digoxin lowers the chronotropic effect (lowering HR) and
the dromotropic effect (slower impulses through AV nodes to lower
HR). An increased inotropic effect plus a reduced chronotropic and
dromotropic effect together increases the stroke volume and,
therefore, cardiac output (cardiac output= stroke volume * HR).

Digoxin is toxic. Nurses must continually monitor if the bloods show

digoxin is within 0.5 to 2 ng/ml. Nausea, anorexia, and vision changes
(blurry or halos) are common A/Es when digoxin exceeds 2 ng/ml.
Digiband is the antidote.

Nurses must always check the apical pulse before administration. The
apical pulse is located in the 5th intercostal space, inferior to R) nipple
and lateral. Stop digoxin if the apical pulse is <60, 70, 90 for adults, kids,
and infants.

Risky for digoxin >2 ng/ml when the patient is hypokalemia<3.5

(especially when the patient is on loop diuretics like furosemide and
thiazide), but digoxin self does not cause hypokalemia.
Hypomagnesemia <1.5 or hypercalcemia >10.2. CCBs directly increase
the digoxin level. The electrolyte imbalance is more likely in renal
patients (BUN 5-20, creatinine 0.6-1.2) or elderlies as their renal and
hepatic function is compromised.

Educate the patients to always take their apical pulse BEFORE taking
digoxin (60, 70, 90 for adults, kids, and infants). Educate the patients to
closely monitor the A/Es like nausea, vomiting and vision changes for
digoxin toxicity. Encourage patients to take more K+ food, especially if
they are on loop diuretics like furosemide which lowers the K+.

To conclude, beware of ATP- Apical pulse <60bpm. Toxic if digoxin is >2,

manifested as nausea and vision changes, renal patients (BUN 5-20 or
creatine 0.6-1.2) are risky. Hypokalemia (>3.5), especially if the patient
is on loop diuretics like furosemide or thiazide.
Calcium channel blockers are dihydropyridines like amlodipine,
felodipine, and nifedipine are vascular selective (cause vasodilation)
CBBs. Dihydropyridines CCBs indicated to HTN and angina. Non-
dihydropyridines like verapamil or diltiazem are myocardium CCBs have
negative inotropic/chronotropic effects. So non dihydropyridines
indicated to HTN, angina, tachycardia and arrhythmia (works on nodal
tissue and myocytes).

Nurses should regularly

1. monitor patients in case of bradycardia or hypotension especially

when taking non dihydropyridines like diltiazem or verapamil. Diltiazem
and verapamil cant be given with beta blockers.

2. Also be aware of reflex tachycardia (when HR is too low, RAAS might

cause tachycardia as a compensatory mechanism).

3. orthostatic hypotension (low bp when standing up and drowsiness)

as risk of fall and slow movement.

4. Monitoring AV block and CBBs are contraindicated to 2,3 degree of

heart block.

5. Monitoring HF as CCBs especially non dihydropyridines like

benzothiazepine or phenylalkylamine stopes ca2+ goes to the
myocardium so there will be less inotropic effects and thus fluid
retention. So checking the lung sounds (crackles), dyspnea (SOB) or
oedema. Performing daily weight (3ibs/day-5ibs/week)

6. No grape juice (strengthener) as the pharmacological effects can be

too much. Also not concurent with statins which greatly increase the
muscle cramp.

7. Encourage the patients to have high fiber diet as CBBs cause

constipation (bowel not contacting as usual).

8. CCBs directly increase digoxin levels. Monitoring digoxin toxicity (0.5-

2) and manifested as nausia, annorexia, and halos
Nitroglycerin (GTN) is a coronary arteries vasodilator to lower the bp
(preload and afterload) for chest pain (more o2 delivered with blood).
Nitroglycerin contraindicated to phosphodiesterase inhibitors like
Viagra (sildenafil) or Cialis (tadalafil), phosphodiesterase inhibitor plus
nitroglycerin can cause severe hypotension. Nitroglycerin is also
contraindicated to increase intracranial pressure. Wearing gloves when
administrating nitroglycerin as nurses don't want hypotension. Educate
the patient not to take a drink or food or chew the tablet as
nitroglycerin is given sublingually. Headache is likely to happen as an
A/E, means the nitro-glycerine is working.

After giving the nitroglycerin, constantly monitor the BP and the chest
pain. Administrate the second dose after 5 mins if the chest pain stays
and BP is above 90 and lower less than 30. Administrate the third dose
if symptoms remain for spray prime five times before administration.
Stop if the systolic is lower than 90 or lower by 30. Facial flushing,
tingling under the tongue, and dizziness are common harmless A/Es.
Nitroglycerin IV MUST needs an infusion pump to give the medication
precisely, usually they got a hemodynamic monitor. Apply nitroglycerin
patch on no hair/fat tissue of the upper torso or arms. Put patch on
different position next time. No remove when headache shows. The
body will tolerate it. Applying the patch less than 14 hours per day and
must remove it during sleeping to prevent tolerance.
Loop diuretics like frusemide or bumetanide work by inhibiting sodium-
potassium-chloride (Na-K-CI) cotransporters ions in the loop of Henle in
ascending limb of kidneys to reabsorb ions (Na+, K+, Mg+) and water
follows. Loop diuretics are indicated for HTN, HF, oedema, liver
impairment (while ascites), and hypercalcemia. Monitor hypocalcaemia
<8.5, hypomagnesemia <1.5, hypokalaemia <`3, hyponatremia <135
(hyponatremia causes lithium toxicity, 0.5-1.2). Orthostatic
hypotension. Giving frusemide IV very slowly as fast frusemide can
cause ototoxicity (ear toxic). Watch for dehydration, daily weights, BSL
and gouts. Always check bp before administration. Pt need to limit fluid
intake. Frusemide onset of action 5-10 mins, peak plasma 30 mins, half
life 2 hrs, medication effects 2-4 hrs, therapeutic effects 6 hrs.
Thiazide like hydrochlorothiazide works by inhibit sodium-chloride (Na-
CI) cotransporter in distal convoluted tubule to reabsorb ions. (Loop
diuretics are five times more potent because the loop of Henle is
responsible for 25% Na+ reabsorption, and the distal convoluted tubule
is responsible for 5%). Indicated to HTN, HF, and kidney calculi (kidney
stones). Beware of HYPERCALCEMIA (calcium is now all in blood from
the kidneys, and that’s why hydrochlorothiazide indicates renal calculi),
hyperglycaemia (70-100) and hyperuricemia (more density due to less
fluid, >7) hypokalemia (triggers digoxin toxicity), hyponatremia (135-
145, lithium toxicity, 0.5-1.2). pt need to limit fluid ntake.
Potassium sparing diuretics works on distal tube and collecting duct.
the diuretics indicate to HTN, HF, oedema, hyperaldosteronism and
hypokalemia (concurrent with loop/thiazide diuretics). Potassium-
sparing diuretics are contraindicated to renal failure and need to
monitor renal function like creatine or BUN.

Type 1, epithelial sodium channel inhibitors like amiloride or

triamterene stop sodium from entering the epithelial sodium channel
(where the sodium-potassium exchange pump is) in the distal tubule
and collecting duct. So sodium would stay in the filtrate into the urine,
and potassium stays in the blood (hyperkalemia).

Type 2, Aldosterone antagonists=Mineralocorticoid receptor

antagonists (MRAs)=Anti mineralocorticoid

Aldosterone directly makes kidneys increase sodium reabsorption and

increases the number of sodium-potassium exchange pumps in
epithelial sodium channels. Aldosterone antagonists like spironolactone
or eplerenone keep sodium in filtrate and potassium in the blood.
Spironolactone also indicates to hyperaldosteronism (making too much
aldosterone).

Monitor fluid balance and daily weight. Checking BP before medication

administration. Sometimes concurrent with ARBs/ACEIs, so monitor
hyperkalemia. Also, lithium toxicity (0.5-1.2, potassium sparing diuretics
lower lithium clearance). Spironolactone can cause hormone disorders
and sexual dysfunction. Pt need to limit fluid intake.
Heparin, an indirect thrombin inactivator, slows the blood clotting
process by enhancing the antithrombin 3’ effect (slowing thrombin
activation hence fibrinogen to fibrin conversion). Heparin indicates
venous thromboembolism (DVT and PE), MI, ischemic stroke, Afib
(blood not being properly pumped and therefore stasis), and clot
prevention after surgeries.

Heparin dose is dependent on pt weight and aPTT. A therapeutic range

of aPTT (drawn for the test every 4-6hrs) is 60-80s (the number could
be various, but 1.5-2.5 times of pt normal aPPT). If aPTT is too low, then
increase the drip rate. If the aPTT is too high, hold the heparin drip for
an hour, then restart with a lower dose. If given in subcut, avoid scar
(2.5cm) or umbilical (5cm) area. Dont message the injection area.

Monitoring CBC (low hbg/hct- haemoglobin/hematocrit refers to blood

loss, hematocrit is the ratio of blood and haemoglogin, around 40% ),
gum oozing, melena (a positive stool guaiac test indicates GI bleeding),
hematuria, hematemesis (or coffee ground emesis), tachycardia and
hypotension (internal bleeding-relative hypovolemic shock), severe
headache (intercranial bleeding/haemorrhagic stroke), heparin-induced
thrombocytopenia (immune system attacks heparin and forcibly active
platelets making tiny clots that could block the blood supply to organ,
similar to dissemination intravascular coagulation). Swap to argatroban
if A/Es show. Protamine is the antidote. Heparin can cause
osteoporosis.

Can swap to direct thrombin inhibitor like argatroban.

Sometimes pt starts heparin first, then warfarin (onset in 5 days?) after

INR reaches the INR therapeutic range 2-3 (usually 1). Heparin is ok
during pregnancy, not warfarin.
Warfarin (coumadin) is a vitamin K (used by the liver to make clotting
factors) antagonist. Warfarin inhibits clotting factor 1(0)972. Warfarin
starts to work after five days and should be given same time every day.
Monitoring tachycardia and low BP (internal bleeding? Watch for CBC-
hemoglobin and hematocrit- hemoglobin/blood ratio-40%), gum
oozing, melena (a positive stool guaiac test refers to GI bleeding),
hematuria, severe headache (intercranial bleeding/haemorrhagic
stroke), and hematemesis (or coffee ground emesis). Vitamin K is the
antidote, so be aware of the food intake that reverses warfarin’s effect.
When giving warfarin, the therapeutic range of INR should be 2-3.
Warfarin cant be given during pregnancy. Warfarin has a tablet form,
not like heparin. Try not use IM route as increase the risk of bleeding.
Swap to phenindione which is a Vitamin K antagonist.
Statin (atrovasatin-lipitor, zocor-simvastatin) is an HMG-COA reductase
inhibitor. HMGCOA is an enzyme for LDL synthesis. Due to incomplete
LDL synthesis, the body would remove LDL from the bloodstream to the
liver and increase the number of HDL to help with the removal. Stains
indicate high cholesterol levels (total 5 or LDL>3.4/100, HDL<1/60),
slowing atherosclerosis and stabilising the plaque. Statins might cause
muscle pain/weakness and manifest as an increased level of creatine
kinase in the blood (creatine kinases are only supposed to be in
muscle). A sustained high creatine kinase level (CPK) can induce
rhabdomyolysis (muscle degraded). During rhabdomyolysis, myoglobin
is released into the blood and blocks the tubules in the kidneys, causing
renal failure. Concurrent statin with fenofibrate/gemfibrozil (lower
triglycerides) increases the risk of rhabdomyolysis. Contraindicated to
grapefruit. Monitor ALT/AST, an enzyme converting proteins into
energy for liver cells and a high level indicates liver failure. Statin can
cause hyperglycaemia in patients with DM. Statin concurrent with
calcium channel blockers increases the muscle cramp risks.