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CARDIOLOGY STUDY GUIDE 2025
Cardiogenic Shock -
1. CO decreases (cardiac index)
2. Vasoconstriction -- inc SVR (afterload )
3. Inc preload (PWCP )
4. Inc CVP
Cardiovascular effects of thyrotoxicosis -
High output failure
--> HTN comes from a decrease in SVR BUT an increase in contractility...
Causes of QT prolongation -
Tx for Jarvell = Beta blocker and pacemaker...
Dihydropyridine Ca2+ channel blockers sideffect
[Amlodipine, nifedipine, nimodipine (used in subarachnoid hemorrhages to prevent vasospasm) -
Peipheral edema
Hemodynamics measurements in shock -
1) Septic shock
- underlying infection
- Decreased SVR (*reduced afterload*), decreased Right atrial pressure, pulmonary artery pressure,
and PCWP pressure (lack of flow back to heart; that is an IN ORDER reason why those are all low)
- Decreased/low normal PCWP
- Capillary leakage --> decreased preload
-Elevated MVO2 (poor gas exchange at capillaries because heart pumping fast, and no
vasoconstriction)
2) Neurogenic shock
- Loss of vagal tone
- Hypotension
- Bradycardia is classic (impaired sympathetic response )
- Low MVO2 (great gas exchange since blood is moving so slowly through tissues )
3) Cardiogenic shock
- May be 2/2 MI OR post-op cardiac tamponade
- impaired LV contractility --> reduced cardiac index (CI )
-failure of forward slow of blood --> pulmonary edema and increased PCWP (LA pressure) +
hypotension
- systemic vasoconstriction leading to cool extremities
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4) Anaphylactic (distributive) shock is classically associated with high cardiac output, low
peripheral vascular resistance, and low pulmonary capillary wedge pressure. Anaphylaxis is
a clinical diagnosis due to an allergic reaction causing dysfunction of 2 organ systems.
Cardiac tamponade -
POST CABG leading to cardiogenic shock
*Elevated and equilibrated intracardiac diastolic pressures* on cardiac cath
F/U Echo for dx
Tx: pericardial window
Pretest probability of coronary artery disease -
Use this chart and see next slide for algorithm
Atypical --> unrelated to physical activity
Evaluation of chest pain -
Women < 50 w/ atypical chest pain and a normal ECG do not require any further testing...
Evaluation of chest pain in the emergency department
-
Relative frequency of selected presenting symptoms in acute coronary syndrome -
Chest pain 80-85%
Dyspnea 70-75%
Nausea 40-55%
Vomiting 15-20%
Epigastric pain 10-15%
ECG should always be done first if ACS is a possibility, even if GI sx seem more likely
Differential diagnosis & features of chest pain -
Esophagus --> Normal ECG/ces, CP that is substernal and radiates to neck
Takayasu arteritis -
BP difference b/t L and R arms
Nitrates -
Used for MI Function:
- dilates Veins, Arterioles, and coronary arteries -
dilating veins -- decreased preload and LVED - reduce
O2 demand by decreasing wall stress.
Medications to withhold prior to cardiac stress testing -
Hold antianginal agents 24-48 hours prior if trying to Dx CAD
- Beta blockers
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- Ca2+ channel blockers
- Nitrates
If trying to see if the antianginals are working in prediagnosed CAD you obviously would not hold
these
MOA Stress test -
Adenosine/dipyridamole --> augments flow through healthy vessels; less flow through
diseased vessels
Test of choice for AAA -
Abd U/S
AV Fistula 2/2 trauma -
MC is a lower extremity fistula
- shunting of blood to venous side increases SVR, *increases preload*, increases CO
- wide pulse pressure
- brisk carotid upstroke
- systolic flow murmur
- tachycardia
- flushed lower ex
- LVH
*high output cardiac failure*
Pt experiences progressive weakness and exertional dyspnea
Dx: Doppler US
Reentrant Ventricular Arrhythmias (ventricular fib) - -
Common in immediate post MI (first hour)
- responsible for sudden cardiac arrest (*MCC* )
See a pt w/ ST segment elevations --> MI --> Syncopal episode --> Sudden cardiac arrest --> the cause
of the syncope is V.Fib
Immediate Phase 1a Ventricular Arrhythmias: within 10 min. Predisposes reentrant
arrhythmias Delayed phase 1b: 10-60 min after MI. Abnormal automaticity. ECG: Vfib/ Vtach
Tx: immediate defib / CPR / Epi / amiodarone
V tach 2/2 Diuretics -
Pt gets put on furosimide and experiences v tach
*CHECK ELECTROLYTES, check serum digoxin level.*
Furosimide can cause hypok and hypomg
If on digoxin, hypok can potentiate side effects
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Approach to adult cardiac arrest -
Approach to sinus bradycardia in adults -
Atropine
F/U Epi, DA, or transcutaneous pacing
Cor Pulmonale -
Smoking hx
Cough
JVD
Decreased breath sounds
CXR: enlarged central pulmonary arteries w/out evidence of vascular congestions
RF: COPD, Lung disease, PVD, OSA
Sx: dyspnea on exertion, exertional syncope (dec CO), exertional angina (inc myocardial demand)
PE: Peripheral edema, inc JVD (a wave), loud S2, right sided heave, pulsatile liver due to congestion,
hepatomegaly, tricuspid regurgitation murmur. Possible ascites
Imaging: ECG: RBBB, R axis D, RVH, RAE,
ECHO: TC regurgitation, pulm HTN, dilated RV
Heart cath: gold standard showing RV Dysfunction, pulm HTN (*pulmonary systolic pressure >25*)
PDE-5 inhibitors + ? = no beuno -
Nitrates & alpha-blockers
Acute arterial occlusion 2/2 PAD -
Signs of Acute limb ischemia:
Rest Pain, pallor, poikilothermia, paresthesias, pulselessness, paralysis, muscle weakness
RF: afib -- left atrial thrombus -- thromboembolic occlusion
Tx: *IV HEPARIN* immediately
DO NOT ORDER DOPPS 1st --> this ia a limb threatening situation
PAD w/ intermittent claudication is indicative of ... -
a 20% 5-year risk of non-fatal MI or stroke 15-30 %
risk of death due to cardiovascular causes
Renovascular Disease -
Dec in BF to the JGA --- inc RAAS --- HTN
MCC of secondary HTN
Causes: Atherosclerosis, Fibromuscular dysplasia
Downloaded by NELSON KIIRU ()
CARDIOLOGY STUDY GUIDE 2025
Cardiogenic Shock -
1. CO decreases (cardiac index)
2. Vasoconstriction -- inc SVR (afterload )
3. Inc preload (PWCP )
4. Inc CVP
Cardiovascular effects of thyrotoxicosis -
High output failure
--> HTN comes from a decrease in SVR BUT an increase in contractility...
Causes of QT prolongation -
Tx for Jarvell = Beta blocker and pacemaker...
Dihydropyridine Ca2+ channel blockers sideffect
[Amlodipine, nifedipine, nimodipine (used in subarachnoid hemorrhages to prevent vasospasm) -
Peipheral edema
Hemodynamics measurements in shock -
1) Septic shock
- underlying infection
- Decreased SVR (*reduced afterload*), decreased Right atrial pressure, pulmonary artery pressure,
and PCWP pressure (lack of flow back to heart; that is an IN ORDER reason why those are all low)
- Decreased/low normal PCWP
- Capillary leakage --> decreased preload
-Elevated MVO2 (poor gas exchange at capillaries because heart pumping fast, and no
vasoconstriction)
2) Neurogenic shock
- Loss of vagal tone
- Hypotension
- Bradycardia is classic (impaired sympathetic response )
- Low MVO2 (great gas exchange since blood is moving so slowly through tissues )
3) Cardiogenic shock
- May be 2/2 MI OR post-op cardiac tamponade
- impaired LV contractility --> reduced cardiac index (CI )
-failure of forward slow of blood --> pulmonary edema and increased PCWP (LA pressure) +
hypotension
- systemic vasoconstriction leading to cool extremities
Downloaded by NELSON KIIRU ()
, lOMoARcPSD|26582732
4) Anaphylactic (distributive) shock is classically associated with high cardiac output, low
peripheral vascular resistance, and low pulmonary capillary wedge pressure. Anaphylaxis is
a clinical diagnosis due to an allergic reaction causing dysfunction of 2 organ systems.
Cardiac tamponade -
POST CABG leading to cardiogenic shock
*Elevated and equilibrated intracardiac diastolic pressures* on cardiac cath
F/U Echo for dx
Tx: pericardial window
Pretest probability of coronary artery disease -
Use this chart and see next slide for algorithm
Atypical --> unrelated to physical activity
Evaluation of chest pain -
Women < 50 w/ atypical chest pain and a normal ECG do not require any further testing...
Evaluation of chest pain in the emergency department
-
Relative frequency of selected presenting symptoms in acute coronary syndrome -
Chest pain 80-85%
Dyspnea 70-75%
Nausea 40-55%
Vomiting 15-20%
Epigastric pain 10-15%
ECG should always be done first if ACS is a possibility, even if GI sx seem more likely
Differential diagnosis & features of chest pain -
Esophagus --> Normal ECG/ces, CP that is substernal and radiates to neck
Takayasu arteritis -
BP difference b/t L and R arms
Nitrates -
Used for MI Function:
- dilates Veins, Arterioles, and coronary arteries -
dilating veins -- decreased preload and LVED - reduce
O2 demand by decreasing wall stress.
Medications to withhold prior to cardiac stress testing -
Hold antianginal agents 24-48 hours prior if trying to Dx CAD
- Beta blockers
Downloaded by NELSON KIIRU ()
, lOMoARcPSD|26582732
- Ca2+ channel blockers
- Nitrates
If trying to see if the antianginals are working in prediagnosed CAD you obviously would not hold
these
MOA Stress test -
Adenosine/dipyridamole --> augments flow through healthy vessels; less flow through
diseased vessels
Test of choice for AAA -
Abd U/S
AV Fistula 2/2 trauma -
MC is a lower extremity fistula
- shunting of blood to venous side increases SVR, *increases preload*, increases CO
- wide pulse pressure
- brisk carotid upstroke
- systolic flow murmur
- tachycardia
- flushed lower ex
- LVH
*high output cardiac failure*
Pt experiences progressive weakness and exertional dyspnea
Dx: Doppler US
Reentrant Ventricular Arrhythmias (ventricular fib) - -
Common in immediate post MI (first hour)
- responsible for sudden cardiac arrest (*MCC* )
See a pt w/ ST segment elevations --> MI --> Syncopal episode --> Sudden cardiac arrest --> the cause
of the syncope is V.Fib
Immediate Phase 1a Ventricular Arrhythmias: within 10 min. Predisposes reentrant
arrhythmias Delayed phase 1b: 10-60 min after MI. Abnormal automaticity. ECG: Vfib/ Vtach
Tx: immediate defib / CPR / Epi / amiodarone
V tach 2/2 Diuretics -
Pt gets put on furosimide and experiences v tach
*CHECK ELECTROLYTES, check serum digoxin level.*
Furosimide can cause hypok and hypomg
If on digoxin, hypok can potentiate side effects
Downloaded by NELSON KIIRU ()
, lOMoARcPSD|26582732
Approach to adult cardiac arrest -
Approach to sinus bradycardia in adults -
Atropine
F/U Epi, DA, or transcutaneous pacing
Cor Pulmonale -
Smoking hx
Cough
JVD
Decreased breath sounds
CXR: enlarged central pulmonary arteries w/out evidence of vascular congestions
RF: COPD, Lung disease, PVD, OSA
Sx: dyspnea on exertion, exertional syncope (dec CO), exertional angina (inc myocardial demand)
PE: Peripheral edema, inc JVD (a wave), loud S2, right sided heave, pulsatile liver due to congestion,
hepatomegaly, tricuspid regurgitation murmur. Possible ascites
Imaging: ECG: RBBB, R axis D, RVH, RAE,
ECHO: TC regurgitation, pulm HTN, dilated RV
Heart cath: gold standard showing RV Dysfunction, pulm HTN (*pulmonary systolic pressure >25*)
PDE-5 inhibitors + ? = no beuno -
Nitrates & alpha-blockers
Acute arterial occlusion 2/2 PAD -
Signs of Acute limb ischemia:
Rest Pain, pallor, poikilothermia, paresthesias, pulselessness, paralysis, muscle weakness
RF: afib -- left atrial thrombus -- thromboembolic occlusion
Tx: *IV HEPARIN* immediately
DO NOT ORDER DOPPS 1st --> this ia a limb threatening situation
PAD w/ intermittent claudication is indicative of ... -
a 20% 5-year risk of non-fatal MI or stroke 15-30 %
risk of death due to cardiovascular causes
Renovascular Disease -
Dec in BF to the JGA --- inc RAAS --- HTN
MCC of secondary HTN
Causes: Atherosclerosis, Fibromuscular dysplasia
Downloaded by NELSON KIIRU ()
