CARDIOLOGY

Surface anatomy
 • HTN is also known as silent killer
• Uncontrolled elevated BP levels
produce a variety of additional
complications, including heart failure,
renal failure, dissecting aneurysms,
PVD, retinopathy, and stroke.

ANGINA

Unstable angina stable angina Prinzmetal angina

occurs at rest without any angina occurs during exercise caused by a vasospasm of
obvious precipitating factors or activity. coronary ar- teries in the
or with minimal exertion. absence of occlusive disease.
When patients experience
Patients with this type of
episodes of stable angina,
angina respond to NTG for
immediate medical exercise must be terminated short-term management of
intervention, because the and HR and BP need to be their chest pain.
patient is at impending risk for taken to determine the RPP
pharmacological choice is a
further complications such as (RPP = HR × SBP). In
calcium channel blocker to
an MI or a lethal arrhythmia addition to terminating
reduce the influx of calcium
(V-tach or V-fib) exercise and resting,
into the smooth muscle cells
of the coronary arteries and
reduce vasospasm.

MYOCARDIAL INFRACTION

The term injury illustrates the The major complications The ultimate complication
presence of a new MI, whereas following an MI are recurrence would be cardiogenic shock
the term infarction depicts an of ischemia, LV failure, and with inadequate CO and
old heart attack with dead ventricular arrhythmias. insufficient arterial BP to
tissue that cannot be reversed. perfuse the major organs as a
Therefore, when a patient is result of severe LV failure.
said to have had a complicated
irreversible changes start to MI, it is indicative that medical interventions such as
appear 20 minutes to 2 hours ischemia, LV failure, or the intra-aortic balloon pump
from the onset of myocar- dial significant ventricular (IABP)
ischemia.3 arrhythmias have developed.
The IABP is a balloon catheter
Angina commonly precedes an In the acute post-MI period. placed within the aorta that
MI, but the intensity of the Ischemia after MI is inflates during diastole,
symptoms is dramatically particularly important because thereby increasing coronary
increased. it indicates that there may be artery perfusion, and deflates
vulnerable myocardium with a during systole, thereby
reduced oxygen supply that decreasing afterload
may go on to infarct

ST E MI (ST elevated MI) NON- ST E MI

 Pt cant complete R wave  If somebody had MI- u take them to
 Complete loss hospital withing 30 mins- symptoms
of myocardium- can be revered
 CO severely  Its not completely blocked
affected- coz  Unstable angina is seen
flexibility is loss  Q wave not seen
 Occurs when CA completely blocked Causes-
 Wen chest pain- take to hospital – n check Infarction
ECG-
 If Q wave- full thickness infraction  BP- will not be high at rest (HR will
 If no Q wave-not severe problem inc but slight just to inc demand- so
After a month of rehab- patient has dead issue will not cause inc BP)
inside  SV- decrease cox of poor strength
 HR- increase- coz body demand is same-  CO- less than what it use to be coz
but only 80 % of heart is working only 80% is working
 LVE DV- normal- after 5 yrs- LV  RPP- inc
hypertrophy- loses flexibility- DyHF  MAP- LOW
 EF- down  ECG- ST elevation
 Heart sound- S4 (if hypertrophy)
 Auscultation- normal
 Sao2/spo2- mayb normal until the HB
reduces in long run

DRUGS USES:
MEDICATION MEDICATION EFFECT PT CONSIDERATION

Diuretics Water pills- reduces plasma Dizzy and

Antihypertensive drug Light headed with postural
change

Beta blocker Decreases the work of the restricts HR response to

heart. exercise

anti-anginal,
antihypertensive,
antiarrhythmic,

Calcium channel blocker anti-anginal, dizziness, coughing,

antihypertensive, and wheezing, and swelling of the
antiarrhythmic effects lower limbs

relaxes
blood vessels, and increases
the supply of blood and 0 2 to
the heart

ACE-inhibitor Antihypertensive, vasodilator, Light-headedness and

and used in patients with dizziness, especially with
CHF or with a Ml exercise or hot weather.
Frequent dry, irritating cough

Nitroglycerin Used for treatment of angina Ensure patients carry their

nitroglycerin with them if
reducing myocardial wall they have frequent angina
tension,

Heparin Warfarin Anticoagulation therapy Patient is prone to bruising

(clot-preventing medication) and bleeding

Statin Atorvastatin Lipid-lowering medications Patient may c/o myalgias,

myopathy, and
rhabdomyolysis
 Pain medications Morphine Pain control light headedness, dizziness,
nausea, vomiting, weakness,
confusion, hallucination, and
suppressed ventilation
Corticosteroids
osteoporosis (long term use)

STERNAL PRECAUTIONS

Heart failure-
Left HF Right HF
Shortness of breath- due to pulmonary edema Jugular vein distension
cough Peripheral edema
Dyspnea, dry cough, orthopnea, nocturnal Dependent edema
dyspnea Ascites
Rales and wheezes Sudden weight gain
liver enlargement
Restlessness Anorexia
Confusion Nausea
irritabiloty Bloating
S3 S3
Murmurs of mitral or tricuspid Murmur of pulmonary or tricuspid
insufficiency
SYSTOLIC HF
 Wen muscle don’t contract- sy HF
 If muscle weakness- getting 100 ml (preload)-
but giving out (SV)- 50 ml- but don’t pump out
blood (so backflow)
 So rest of the blood will go back to lung- causes
SYSTOLIC HEART FAILURE (ms cnt contract
enuff to foward all the blood )
 LV getting blood from leg to RA
Reasons
• h/o MI- not able to contract
• receive blood but cant pushes it out
• poor EF- systolic heart failure
• inc Afterload- SyHF
• AF related to cardio output- systolic HF
DYSTOLIC HF
• Hypertrophied valves- not expanding- doesn
mean blood stop coming the heart
• But LV – taking only less blood eg- 70 ml
coming but LV is just taking 50 ml
• So rest will be going back to LA
• From LA- to lungs back
• Not relaxing – DyHF
REASON-
• Hypertrophy- causes dec LVE DV
• LVE DV is preload
HTN pt develeop hypertrophy after 10 -15 yrs- develop
DyHF
  New heart- they cut all the nerves around it- so no sympathetic & parasympathetic
control
 FRANK- STARLING MECHANISM- fill heart with more blood more stronger
contraction- less blood less contraction- so its based on stretch reflex
 Stretch reflex- wen filling complete- stretch receptors- they automatically contracts-
and pushes the blood out and relaxes
 No angina coz no nerve
 Exercises- prolong warm up period- coz stretch reflexes will take time to activate

Exercise tolerance test-

• A positive ETT indicates that there is a point at which the myocardial oxygen supply is
inadequate to meet the myocardial oxygen demand, and the test is therefore positive for
ischemia.
 • A negative ETT indicates that at every tested physiological workload there is a balanced
oxygen supply and demand
• A false-negative ETT is one that is interpreted as negative but the patient in fact has
ischemia.
• A false-positive ETT is one that is interpreted as positive but the patient does not have
ischemia.

CABG- CRADIAC REHAB

PHASE 1-
 Sternal precautions
 Day 1- FITT principle- freq, intensity, time, type

Intensity Rest HR- 101- upto 20 beats above RHR- it go don’t put too much
pressure
 1. Upto 20 beats
2. MET= 1 MET- 3.5 ml /kg/min eg. If 50 kg- it will inc 50 times
Stage 1- go upto 5 MET- will use O2 in MET (for regular ADLs 5 MET/ 9
MET functional capacity )
Time 15-20 mins (pt initially cant do so long)
So start with now much pt can do at the end 15-20 min is enuff frequency
Frequency Initially if just 2-3 mins (breakdown the exercise 2-3 times a day)
Gradually increase in preganancy- coz he is just not able to do 15-20 mins
But if do more- need not have to stop it
E eryday 7 days/ week
Type Walk or arm exercises
GOAL- is to achieve ADL activity-
 Phase 1- 1:1 exercise : rest (6 mins: 6 mins)
 Phase 2- 10:5- (so that heart can be forced to work more
 MET -5 – goal is to achieve- 5-9 MET
Intensity If intensity 40-59 %
Frequency 7 days per week / min 5 upto 7 days / week
Time Duration 30- 60 min at the end of 6 weeks
Type Lower extremities- after 30 mins increase intensity- till 59%
intensity

Intensity Freq Duration

Phase 1- 40 % 7 days 15-20 mins
Phase 2- 40-59 % 5-7 days 30-60
Phase 3- 60-85% 3-5 days 20-60
• If patient has heart transplant/ or on Beta blockers- we don’t relay on HR (maybe VO2 R
OR MAX)
• Rest period- 2:1
•
• If v want to achieve 30 mins for 40 %- but if indivdaul is not able to do it on day 1- np
give him a break/ more frequent break
• Phase 2- goal is 10:5- but if patient needs more break its ok- initially its ok but once we
achieve duration dan slowly decrease rest phase and inc. intensity
• Resistance /Strengthening- after 3 weeks (cardiac rehab), 5 week post (MI)- 8 weeks
(CABG)
• Whole stage 2- is done with ECG connected
• Stage 3 – no need ECG- self monitoring
AAA- Causes-
 Aorta goes down and at the abdominus it bifurcates- and further follows as iliac artery
 Due to increase pressure- any party of aorta will bulge- may be sitting posture or
collecting blood- it may burst some day- no blood flow to legs- can cause paralysis of leg
  If it happens in aortic arch- aortic arch aneurysm
 Abdominal aortic aneurysm- gives referred pain to surrounding tissue, that’s by pain in
low back or groin
 Wen measuring- we can feel the pulse at abdominus (inc CO, SV, BP)

Precautions -
 No holding breath – no close glottis eg- lift weight- we contract abdominus (specially
wen weight is more)
 So when patient becomes too tired, too much pressure on abdominals- more muscle
contracts- inc pressure- well compresses the vessels from inside (vasoconstriction)- INC
BP